Chapter 24

Anesthesia for Cardiac Surgery

Margaret A. Contrera, Melissa Patterson and Mary Cushing

Despite advances in prevention and treatment, cardiovascular disease (CVD) remains the leading cause of death globally, accounting for 30% of mortality. The World Health Organization estimates that CVD will remain the predominant cause of mortality, resulting in 23.6 million deaths by 2030, mostly from coronary artery disease (CAD).¹ In the United States, CVD causes 1 of every 2.9 deaths, half of them due to CAD.² Because of the aging population, degenerative valvular heart disease (VHD) is on the rise. There are currently over 290,000 heart valve operations performed annually worldwide, and that number is expected to triple by 2050, reaching 850,000.³ Both CAD and VHD lead to heart failure, which impacts more than 5 million Americans. The mortality rate for symptomatic patients is a staggering 45%, worse than that of most cancers.⁴ The Centers for Disease Control and Prevention estimates that $444 billion, or $1 out of every $6, in health care costs is spent on cardiovascular disease treatment.⁵

Clearly CVD presents an enormous public health burden. Scientific and medical communities, together with governmental agencies, have worked tirelessly to improve this situation. Consequently, new knowledge about these diseases is accumulating exponentially and technologic advancements have led to the development of cardiac procedures that were once inconceivable. Percutaneous techniques, hybrid operating rooms, mechanical assist devices, robotics, and minimally invasive technology now play significant roles in the practice of cardiothoracic anesthesia. The field has become more diverse, exciting, challenging, and rewarding than ever before.

Care of these high-risk patients in regard to the complex, ever-evolving surgical procedures may at first seem intimidating. But as Richard Morris, a pioneer in the field of cardiothoracic nurse anesthesia advised, “It’s simple really; just manage the pump, pipes and volume.” Accordingly, the first half of the chapter is about general cardiac surgery. It begins with a brief overview of the key physiologic principles that form the foundation of the evidence-based anesthetic management strategies for cardiac surgery. Next, cardiopulmonary bypass (CPB) is discussed, including a description of the circuit components and the physiologic implications of bypass. Then each phase of the perioperative period is examined and the anesthetic implications detailed. The second half of the chapter covers anesthetic considerations for specific cardiovascular diseases and procedures. The pathophysiology of CAD and VHD is briefly reviewed, and anesthetic management of traditional myocardial revascularization and valvular surgery is detailed. New technologic advancements have changed the landscape of cardiac anesthesia. Consequently, the next sections are devoted to management of first, the innovative, minimally invasive approaches that are now used for both valvular surgery and myocardial revascularization. This is followed by a discussion of the devices and procedures that are bringing new hope to the management of end-stage heart failure. The chapter concludes with the anesthetic management of procedures on the ascending aorta and arch that require CPB, including the considerations for deep hypothermic circulatory arrest.

Anesthetic Management of General Cardiac SuRgery

Key Physiologic Principles

Appropriate management of the cardiac surgical patient begins with a comprehensive understanding of normal cardiac anatomy, physiology, pharmacology, and monitoring, as well as the pathophysiologic response to disease. The reader is advised to review the excellent discussions of these topics found in Chapters 13, 16, and 23 as background for the information presented in this chapter. Nevertheless, there are certain key principles that apply to most cardiac surgical patients. An imbalance in myocardial oxygen supply and demand, often as a result of CAD, leads to ischemia or infarction. As a result of the imbalance, the left ventricle hypertrophies by thickening or dilating. The abnormal pressure and volume loads caused by stenotic and regurgitant valves likewise causes the ventricle to compensate by altering its structure, function, and neurohormonal balance. Although each disease starts with a different etiology and pathophysiologic process, with progression of the disease, the limits of compensation are reached and severe decompensated heart failure then ensues.

Myocardial Oxygen Supply and Demand

Myocardial injury and/or infarction are the single most frequent complications after cardiac surgery; they are also the primary cause of complications and death that occur in the hospital setting.⁶ Clearly, optimizing the balance between myocardial oxygen supply and demand is of paramount importance (Figure 24-1). Coronary perfusion pressure (CPP) is equal to the aortic diastolic blood pressure minus the left ventricular end-diastolic pressure (LVEDP). The subendocardium or inner third of the heart muscle is at greatest risk for ischemia because it is exposed to the highest pressure, especially at the peak of systole. Normally CPP is autoregulated between a mean arterial pressure (MAP) of 60 to 140 mmHg. Consequently, MAP is the most useful measure of coronary perfusion in the clinical setting.⁷ However, in patients with CAD, flow is no longer autoregulated after it passes the partial obstruction. Instead, perfusion becomes pressure dependent; especially when the MAP drops below 70 mmHg^8,9 (Figure 24-2). Total coronary blood flow is determined by the perfusion pressure gradient, the time allotted for flow, coronary anatomy, and the resistance. Eighty percent of blood flow to the left ventricle occurs during diastole when the pressure is low (Figure 24-3). Diastolic time progressively shortens as the heart rate increases, resulting in decreased time for coronary perfusion at higher heart rates. Note that elevations in LVEDP and heart rate not only decrease myocardial blood supply but also increase myocardial oxygen demand. An increase in heart rate proportionally increases myocardial oxygen demand and decreases diastolic time.⁷ Large epidemiologic studies show that heart rate is an independent predictor for cardiac and all-cause morbidity and mortality in men and women with and without CVD.⁸ Heart rate is also the most significant cause of perioperative ischemia.⁹ Therefore maintaining an adequate aortic mean pressure and a low heart rate is critical, particularly in patients who have CAD or an elevated LVEDP. The ideal heart rate must be determined on an individual basis, but less than 70 beats per minute (bpm) is a reasonable guide.¹⁰ Patients with concentric left ventricular hypertrophy (LVH) have an elevated LVEDP, so they too are best managed with a higher MAP and lower heart rate. Table 24-1 outlines some of the causes and treatments of alterations in myocardial oxygen supply and demand.

TABLE 24-1

Perioperative Management of Alterations in Myocardial O₂ Balance

Causes of Decreased O₂ Supply	Perioperative Management Strategy
Tachycardia (↓ diastolic time)	Keep heart rate relatively low (less than 70 bpm) Deepen anesthesia during stimulating periods
Hypotension	Maintain high normal MAP; consider phenylephrine ↓ anesthetic depth during less stimulating periods and surgical manipulation that causes ↓ MAP
↑ PaEDP	Consider nitroglycerin Evaluate LV volume with TEE (PaEDP can be falsely elevated in patients with concentric LVH)
↓ O₂ Content	Maintain Sao₂ at greater than 95%
Anemia	Maintain adequate hemoglobin
Causes of Increased O₂ Demand	Perioperative Management Strategy
SNS stimulation	Maintain adequate depth of anesthesia Anticipate stimulating events and treat preemptively.
Tachycardia	Keep heart rate relatively low (less than 70 bpm) Consider β-blockers
↑ Preload	Consider nitroglycerin or diuretic to decrease
↑ Contractility	Consider agents that depress contractility (β-blockers/volatile anesthetics)
↑ Afterload	Avoid hypertension; consider vasodilator

↓, Decreased; ↑, increased; bpm, beats per minute; LVH, left ventricular hypertrophy; MAP, mean arterial pressure; PaEDP, pulmonary artery end-diastolic pressure; Sao_2, saturation of arterial oxygen;

TEE, transesophageal echocardiography.

FIGURE 24-1 Myocardial oxygen supply and demand balance. Heart rate and left ventricular pressure affect both supply and demand. AoDP, Arterial diastolic pressure; LVEDP, left ventricular end-diastolic pressure; Sao₂, arterial oxygen saturation. (Reprinted with permission from Cleveland Clinic Center for Medical Art & Photography © 2006-2012. All rights reserved.)

FIGURE 24-2 Pressure-flow relations of the subepicardial and subendocardial thirds of the left ventricle in anesthetized dogs. In the subendocardium, autoregulation is exhausted and flow becomes pressure dependent when pressure distal to a stenosis declines to less than 70 mmHg. In the subepicardium, autoregulation persists until perfusion pressure declines to less than 40 mmHg. Autoregulatory coronary reserve is less in the subendocardium. (Redrawn from Guyton RA, et al. Significance of subendocardial ST segment elevation caused by coronary stenosis in the dog. Am J Cardiol. 1977;40:373.)

FIGURE 24-3 Blood flow in the left and right coronary arteries. The right ventricle is perfused throughout the cardiac cycle. Flow to the left ventricle is largely confined to diastole. (From Berne RM, Levy MN. Special circulations. In: Berne RM, Levy MN, eds. Physiology. St. Louis: Mosby; 2003.)

Ischemia Cascade

Myocardial ischemia leads to a cascade of events as shown in Figure 24-4.¹¹ It is important to emphasize that diastolic dysfunction precedes systolic dysfunction, and that regional wall motion abnormalities occur on echocardiography before changes on the electrocardiogram (ECG). An imbalance between myocardial oxygen supply and demand will initially induce diastolic dysfunction, making the ventricle stiff and less compliant. These abnormalities will manifest as an increase in the pulmonary artery end-diastolic pressure (PAEDP); however, multiple studies show that the PAEDP is not specific for ischemia.¹² Systolic dysfunction causes regional wall motion abnormalities that can be readily detected on transesophageal echocardiography (TEE). Consequently, TEE is the most sensitive intraoperative monitor for detecting myocardial ischemia.¹³ The single best ECG lead for detecting myocardial ischemia is V₅, which detects 75% of events, so it is important to ensure that the V (brown lead) of the ECG is correctly placed at the fifth intercostal space anterior axillary line. Combining V₄ or V₅ with lead II and using automated ST analysis further improves ECG sensitivity.^11,13,14

FIGURE 24-4 The ischemic cascade. Pathophysiologic sequence of developing myocardial ischemia correlated with timing of detection using various cardiovascular examinations. (Reprinted with permission from Cleveland Clinic Center for Medical Art & Photography © 2006-2012. All rights reserved.)

Preconditioning, Stunning, and Hibernation

When the heart muscle experiences brief periods of ischemia that last less than 20 minutes, necrosis or cell death is prevented, but reversible contractile dysfunction, known as stunning, can occur and last for several hours.15–17 As a result of stunning, many cardiac surgical patients may require 12 to 24 hours of inotropic support after cardiopulmonary bypass (CPB).

Ischemic preconditioning refers to the phenomenon whereby a short period of ischemia improves the heart’s ability to tolerate subsequently longer periods of ischemic insult.¹⁶ All inhalational anesthetics mimic this preconditioning effect. Consequently, there has been a resurgence of inhalation anesthesia as a primary technique for cardiac surgery, especially in patients with near-normal ventricular function. In past decades, there was a concern that the vasodilatory properties of isoflurane caused coronary steal.¹⁸ However, clinical studies have shown that if blood pressure is controlled, ischemic episodes do not increase and outcomes are unchanged when inhalation agents, including isoflurane, are used.^19–21

When stable coronary plaque causes chronic reductions in coronary perfusion, steady-state ischemia occurs, which results in left ventricular perfusion-contraction matching or hibernation. This phenomenon is considered a self-preservation mechanism whereby left ventricular contractile function is reduced to match the amount of oxygen available.22,23 Unlike stunned myocardium, patients with hibernating left ventricles (LVs) often have significantly improved function after CPB and coronary artery bypass grafting (CABG). Differentiation of ischemic myocardium that is considered “viable” is important because approximately 20% to 40% of patients with chronically ischemic LV dysfunction will have a significant improvement after revascularization.^23,24 Multiple nuclear imaging tests and dobutamine stress echocardiography are used to help determine the presence of ischemia and viability. Some of the more common cardiovascular tests that are performed to identify ischemia and viability studies are outlined in Table 24-2.

TABLE 24-2

Significant Findings on Cardiac Preoperative Testing

↑, Increase; +, with; − without; ACS, acute coronary syndrome; AECG, ambulatory electrocardiogram; BBB, bundle branch block; CAD, coronary artery disease; ECG, electrocardiogram; HR, heart rate; L, left; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; LVH, left ventricular hypertrophy; NSTEMI, Non-ST elevation myocardial infarction; PAC, pulmonary artery catheter; PCI, percutaneous coronary intervention; PET, positron emission tomography; PFO, patent foramen ovale; RV, right ventricle; SPECT, single-photon emission computed tomography; STEMI, ST elevation myocardial infarction.

The need to balance myocardial oxygen supply and demand is not limited to patients with CAD. Angina and myocardial infarction in patients with normal coronaries were demonstrated as far back as 1959.²⁵ Many other patients, such as those with chronic hypertension, aortic stenosis, or obstructive cardiomyopathy, will also benefit from a relatively high perfusion pressure and low heart rate. This is because of the structural, functional, and neurohumoral changes that occur in the ventricle in response to ischemia, infarction, and/or abnormal pressure or volume loads.

Heart Failure

Heart failure is a complex pathophysiologic process that causes a clinical syndrome characterized by pulmonary congestion resulting from the heart’s inability to fill with or eject blood in a sufficient quantity to meet tissue requirements.²³ The heart was once thought of as simply the pump of the circulatory system, but it is now known that it evolves into “an endocrine organ” under stress, actively secreting neurohormonal factors in an attempt to meet the needs of the body. For example, atria natriuretic peptide (ANP) is released from the atria in response to volume overload and B-type natriuretic peptide (BNP) is released primarily from the ventricle in response to increased wall stress. These peptides help protect the myocardium by inducing physiologic effects such as diuresis, natriuresis, and vasodilation.²⁶ In fact, BNP has been recognized as a powerful biomarker for diagnosis, determination of severity, and prognostication of heart failure.²⁷ Heart failure is caused by an insult that alters perfusion and leads to a state of neurohumoral imbalance. Activation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS) induces a host of pathologic responses. Consequently, many patients will receive multimodal drug therapy aimed at interrupting the response and slowing disease progression ⁴ (Figure 24-5). Beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and aldosterone antagonists can have a synergistic effect when combined with anesthetics. Although dealing with the resulting vasodilation and/or myocardial depression can be challenging for the anesthetist, medications used to control the patient’s heart failure should be continued in the perioperative period because their benefit is well documented.^23,26–28 In fact, on the basis of multiple large-scale randomized, controlled clinical trials, it is estimated that 465 lives are saved for every thousand patients treated with a combination of beta-blockers, ACE inhibitors, and aldosterone antagonists.²⁹

FIGURE 24-5 Pharmacologic treatments target the pathophysiologic changes caused by heart failure. Drug mechanisms produce one or more beneficial mechanisms including decreased preload, afterload, heart rate, blood pressure, deleterious ventricular hypertrophy and remodeling, sodium retention, and sympathetic stimulation. They improve renal and peripheral blood flow, reverse remodeling, and inotropicity. (From Jessup M, Brozena S. Heart failure. N Engl J Med. 2003;348:2007-2018.)

Left Ventricular Failure and Remodeling

In the face of sympathetic activation coupled with alterations in perfusion, pressure, and volume, the heart changes its size, shape, and function; that is, it remodels itself in an attempt to maintain cardiac output. Supply ischemia causes an increase in ventricular compliance (dilation) and a decrease in contractility, whereas demand ischemia reduces compliance (stiffening) without initially impacting contractility.22,23 The primary characteristics of remodeling are hypertrophy or dilation, myocyte death, and increased interstitial fibrosis. The clinical impact manifests as a change in systolic and diastolic function. Figures 24-6 and 24-7 help summarize and visualize the process.

FIGURE 24-6 Left ventricular (LV) pressure and volume overload produce compensatory responses based on the nature of the inciting stress. Wall thickening reduces (−), whereas chamber dilation (+) increases, end-systolic wall stress as predicted by Laplace’s law. LV pressure-overload hypertrophy has been linked to heart failure with normal ejection fraction (HFNEF), but LV volume overload most often causes heart failure (HF) with reduced ejection fraction (EF). (From Kaplan JA, Reich JA, Savino JS. Kaplan’s Cardiac Anesthesia: The Echo Era. 6th ed. Philadelphia: Saunders; 2011.)

FIGURE 24-7 Conditions leading to remodeling of the heart and resulting in atrophy or hypertrophy. Depending on the circumstances, remodeling can be normal or pathologic. Pathologic remodeling is associated with a propensity toward decompensation, ventricular dilation, systolic dysfunction, and electrophysiologic changes leading to malignant ventricular arrhythmia. (From Hill JA, Olson EN. Cardiac plasticity. N Engl J Med. 2008;358:1370-1380.)

Systolic Dysfunction: As demonstrated in Figure 24-7, A, supply ischemia resulting in myocardial infarction, or chronic volume overload of the left ventricle causes eccentric hypertrophy or dilation. The chamber size increases in an attempt to preserve stroke volume. In the dilated state, the heart loses its normal elliptical football shape and becomes more spherical, resembling a basketball.⁴ In this shape, the heart is unable to contract effectively (systolic dysfunction) and the mitral apparatus is stretched potentially to a point that results in mitral regurgitation (MR). Of patients with heart failure, 35% to 50% will experience MR.³⁰ The degree of systolic dysfunction is commonly expressed as ejection fraction (EF). The EF is calculated as stroke volume (SV) divided by end-diastolic volume (EDV). According to the American Society of Echocardiography’s guidelines, normal EF is 55% or greater, and dysfunction is graded as mild (45%-54%), moderate (30%-44%), and severe (less than 30%). When SV is reduced, the body compensates by activating the SNS to raise the resting heart rate in an effort to maintain cardiac output. Systolic heart failure (SHF) is caused by CAD, dilated cardiomyopathy (DCM), chronic volume overload (regurgitant valves, high output failure), and the later stages of chronic pressure overload (aortic stenosis and chronic hypertension). Myocardial infarction causes regional defects that can eventually encompass the entire myocardium, whereas other causes of heart failure typically reduce global function from the onset.²⁶ As shown in Figure 24-6, SHF is associated with a volume overload of the left ventricle that is managed using multiple drug therapies as shown in Figure 24-5.

Diastolic Dysfunction: Diastolic dysfunction is a more difficult concept to explain, but one that is equally important. Pulmonary congestion and all the symptoms of heart failure can indeed develop with a normal EF. In fact, diastolic heart failure (DHF) is often called heart failure with preserved EF (greater than 40%) (see Figure 24-6). Demand ischemia, resulting from chronic pressure loads from stenotic heart valves, obstructive cardiomyopathy, chronic hypertension, or obesity, causes the myocardium to thicken (concentric hypertrophy) and compliance to decrease (see Figure 24-7).⁴^,284 Pulmonary congestion develops because the fibrosed, nondistensible LV, with an increased LVEDP, is unable to fill adequately despite near-normal systolic function. Diastolic failure is graded class I to IV based on echocardiographic examination findings.³¹ The hypertrophied LV is prone to ischemia; therefore maintenance of a high MAP and slow normal heart rate is crucial.³² Hypotension should be treated promptly, usually with phenylephrine to avoid rapid decompensation that can potentially lead to cardiac arrest. In the hypertrophied heart, chest compressions rarely generate enough pressure to perfuse the noncompliant LV. The mortality and hospitalization rates are similar in both systolic and diastolic failure. Table 24-3 compares the characteristics of patients with systolic and diastolic failure, and Table 24-4 outlines the anesthetic management strategies for systolic and diastolic dysfunction. Oftentimes, as DHF progresses, SHF will develop and the two will co-exist.²⁶

TABLE 24-3

Characteristics of Patients with Diastolic and Systolic Heart Failure

Characteristic	Diastolic HF	Systolic HF
Age	Often in the elderly	Usually 50-70 years
Gender	Often in females	Most often in males
EF	Preserved, greater than 40%	Depressed, less than 40%
LV cavity size	Normal withconcentric LVH	Dilated witheccentric LVH
Chest x-ray	Congestion ± cardiomegaly	Congestion + cardiomegaly
HTN	+++	++
DM	+++	++
Previous MI	+	+++
Obesity	+++	+
COPD	++	0
Sleep apnea	++	++
Dialysis	++	0
Atrial fibrillation	+ Usually paroxysmal	+ Usually persistent
Gallop rhythm	4^th Heart sound	3^rd Heart sound

+, Occasionally associated with; ++, often associated with; +++, usually associated with; 0, no association; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus; EF, ejection fraction; HF, heart failure; HTN, hypertension; LV, left ventricle; LVH, left ventricular hypertrophy; MI, myocardial infarction.

Adapted from Popescue WM. Heart failure and cardiomyopathies. In: Hines RA, Marschall KE. Stoelting’s Anesthesia and Co-Existing Diseases. 6th ed. Philadelphia: Saunders; 2012.

TABLE 24-4

Anesthetic Considerations for Systolic and Diastolic Dysfunction

	Systolic Dysfunction	Diastolic Dysfunction
Preload	Already ↑, avoid overload, especially coming off pump NTG helps reduce preload and ↑ subendocardial perfusion	Volume will be needed to stretch noncompliant LV Evaluate with echo as LVEDP falsely ↑
Contractility	Reduced →, avoid agents that cause further reductions May need inotropic support	Usually good, but caution with agents that suppress function Does NOT tolerate hypotension
Afterload	Reductions will enhance forward flow as long as coronary perfusion pressure maintained SNP works well if volume is adequate	Already ↑ Higher MAP needed to perfuse thick myocardium Treat hypotension aggressively with phenylephrine
Heart rate	Usually high normal due to sympathetic activation	Slow normal to maximize diastolic time for coronary perfusion and ↓ MvO₂ Prone to ischemia Maintain SR →; cardiovert early
CPB	Expect large pump volumes Consider ultrafiltration, diuretic	Pump volume normal

↓, Decreased; ↑, increased; →, therefore; CPB, cardiopulmonary bypass; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial pressure; MvO₂, myocardial oxygen consumption; NTG, nitroglycerin; SNP, sodium nitroprusside; SR, sinus rhythm.

Right Heart Failure

Right heart failure (RHF) is most often secondary to left heart failure (LHF), but can also be caused by pulmonary hypertension or a right-sided infarct. RHF causes systemic venous congestion, hepatomegaly, and peripheral edema.23,26 Management of RHF can be more difficult to manage than left-sided failure because fewer options exist for unloading and supporting the right ventricle. The goal in managing RHF is to improve contractility while reducing right heart afterload. Thus anything that would increase right heart afterload should be avoided, including hypercarbia, hypoxemia, acidosis, and similar conditions that can potentially cause pulmonary hypertension. Nitrous oxide can cause pulmonary hypertension so it, too, should be avoided. Normally the right heart is perfused throughout the cardiac cycle (see Figure 24-3); however, when the right ventricle is distended, coronary perfusion occurs primarily during diastole as it does in the left ventricle.

Cardiopulmonary Bypass

Principles

Most cardiac surgeries must be accomplished with the aid of cardiopulmonary bypass (CPB). The machine is operated by a perfusionist, but it is imperative that the anesthetist have a clear understanding of the components and physiologic impact of CPB. The purpose of CPB is to provide a motionless, bloodless heart for the surgical procedure. This goal is achieved by temporarily diverting venous blood away from the heart to an extracorporeal circulation that adds oxygen and removes CO₂ and then filters it before returning it to the body, most often via the ascending aorta. The CPB circuit is continuous with the systemic circulation and provides artificial ventilation, perfusion, and temperature regulation while diverting the blood from the surgical field. The technique results in stopping nearly all blood flow to the heart and lungs. To stop the heart’s electrical activity and to protect it during the procedure, the heart is intermittently perfused and cooled with a chemical solution called cardioplegia. Although the goal is to provide near physiologic hemodynamics and acid/base balance, the technique is nonphysiologic. A near-normal cardiac index is usually maintained with an arterial flow of 2.0 to 2.4 L/minute/m², but it is nonpulsatile. There is some controversy over what is the most appropriate MAP on bypass, but most advocate no less than 50 to 60 mmHg. Older patients or those with known carotid disease should have a higher MAP, closer to 60 to 70 mmHg, to assure that there is adequate cerebral perfusion pressure.⁹ The patient’s blood and components are exposed to nonendothelial surfaces, which increase the incidence of platelet dysfunction and coagulopathy. CPB incites a host of inflammatory responses; these are outlined after the discussion of the circuit components.

Basic Circuit

The CPB machine consists of five basic components: a venous reservoir, a main pump, an oxygenator, a heat exchanger, and an arterial filter (Figure 24-8). The following is a simple explanation of full CPB: (1) venous (deoxygenated) blood is drained from the right side of the heart and carried by tubing to a reservoir; (2) a pump then propels the blood to (3) an oxygenator and (4) a heat exchanger; and (5) the oxygenated blood passes through a filter before returning to the arterial circulation to perfuse the rest of the body. The modern bypass machine also performs several other functions, including delivering cardioplegia by means of accessory pumps. The heart is vented and blood is salvaged from the field by means of suction devices.

FIGURE 24-8 Components of the extracorporeal circuit. (1) Integral cardiotomy reservoir; (2) membrane oxygenator bundle; (3) venous blood line; (4) arterial blood line; (5) arterial filter purge line; (6) arterial line filter; (7) venous blood pump (also called the arterial pump head; this pump forces venous blood through the membrane oxygenator and arterialized blood to the patient’s aortic root); (8) cardiotomy suction pump; (9) ventricular vent pump; (10) cardioplegia pump; (11) crystalloid cardioplegia; (12) water inlet line; (13) water outlet line; and (14) gas inlet line. (From Davis RB, Kauffman JN, Cobbs TL, Mick SL. Cardiopulmonary Bypass. New York: Springer-Verlag; 1995.)

Cannulae

The CPB circuit includes cannulae and tubing made of medical grade polyvinyl chloride (PVC), with a biocompatible coating to decrease the inflammatory response associated with CPB and to preserve blood components. One or two “staged” (meaning more than one hole to drain the blood) venous cannulae are used to remove the deoxygenated blood from the heart. A large-bore two-stage or multistage cannula that drains blood from both the right atrium and the inferior vena cava is used for CABG and aortic valve procedures in which the heart is actually closed and small amounts of retained blood will not interfere with the surgery (Figure 24-9). Open-cavity procedures, such as mitral, pulmonic, and tricuspid valve surgery, or procedures that repair defects such as atrial septal defects (ASD), patent foramen ovale (PFO) defects, or ventricular septal defects (VSD) all require a bloodless field. For such procedures, two separate venous single-stage cannulae are individually inserted into the superior and inferior vena cava, and the vessels are snared with elastic loops to prevent systemic venous blood from entering the heart (Figure 24-10). This technique is also known as bicaval cannulation.

FIGURE 24-9 Aortic (Ao) and single, double-staged, right atrial (RA) cannulation. Notice the drainage holes of the venous cannula in the right atrium and inferior vena cava. (From Connolly MW. Cardiopulmonary Bypass. New York: Springer-Verlag; 1995.)

FIGURE 24-10 Position for two-vessel cannulation of the right atrium (RA) with placement of drainage holes into the superior vena cava (SVC) and inferior vena cava (IVC). The aortic cannula is not shown. (From Connolly MW. Cardiopulmonary Bypass. New York: Springer-Verlag; 1995.)

Prime

Prime is the fluid used to fill the CPB circuit and components. It is composed of an isotonic balanced electrolyte solution, such as lactated Ringer’s, Plasmalyte-A, or Normosol-R, that closely matches the principal ionic composition of blood. During setup, the perfusionist must take great care to de-air the circuit. Traditionally the priming volume for the CPB is 1 to 2 L. However, the development of minimally invasive cardiac procedures required the use of smaller cannulae and tubing to enable the surgeon to visualize the field. Medications and other solutions are often added to the prime for a variety of purposes; for example, colloid to decrease postoperative edema, blood to treat anemia, mannitol to promote diuresis, heparin to ensure adequate anticoagulation, and bicarbonate to treat acidosis. When the prime fluid is added to the circulating blood volume, a dilutional anemia occurs, and it is not unusual for the hematocrit to fall to 22% to 25%. The dilution offsets some of the increase in blood viscosity that occurs when the blood cools during CPB.

Venous Reservoir

Venous reservoir (Figure 24-8 [1]) CPB is initiated when the perfusionist removes a clamp that occludes the tubing connecting the venous cannulae to the venous reservoir. The venous reservoir is typically hard-shelled and divided into two compartments, one for the venous drainage from the heart and the other for the blood suctioned or vented directly from the surgical field. This portion of the reservoir is known as cardiotomy; it is discussed in detail later. Traditionally blood drains from the patient to the reservoir by gravity. The rate of venous drainage is determined by the size and placement of the cannulae, height of the bed, and the patient’s intravascular volume. With the introduction of minimally invasive techniques, gravity drainage was inadequate due to the small cannulae and tubing, so the practice of vacuum-assist venous drainage (VAVD) was established. A vacuum regulator is added to the venous reservoir with a piece of Y tubing and a pressure of −40 mmHg is applied. This Y tubing is used to turn on the suction or open the system to atmospheric pressure. Improved drainage can facilitate surgical exposure and decrease the necessity of adding more crystalloid and/or blood to the CPB circuit. The inherent risks include hemolysis of blood cells and air embolism. VAVD at a suction of −40 mmHg causes less hemolysis than when the suction is increased to −80 mmHg.³³ It is critical that the fluid level in the venous reservoir be kept sufficiently high to prevent air from entering the main pump and causing an air embolism. An alarm is incorporated into the venous reservoir to alert the perfusionist if the fluid level drops below a specific level. The perfusionist may add fluid and medications to the venous reservoir.

Main Pump

Blood is propelled through the CPB machine by an electrical pump (Figure 24-8 [7]). Two types of pumps are available. A roller pump produces flow by subtotally compressing large bore tubing against a tract and propelling the blood forward. Constant nonpulsatile flow is produced that is directly proportional to the number of revolutions per minute of the roller heads regardless of arterial resistance in the circuit. A centrifugal pump uses a magnetically controlled impeller that rotates rapidly, causing a pressure drop that causes blood to be sucked into the housing and ejected. A major difference between the two pumps is that the flow from the centrifugal pump will vary with changes in preload and afterload. For this reason, a flowmeter must be attached to the arterial side of the pump. The roller pump is economical and simple to use; however, unlike the centrifugal pump, it has the disadvantage of increasing the destruction of blood elements. As a result, centrifugal pumps are replacing roller head pumps in contemporary practice. In the event of a power failure, a hand crank can be used to operate either pump.

Oxygenator

The oxygenator performs the functions of oxygenating venous blood and removing carbon dioxide (CO₂) (Figure 24-8 [2]). In the past, bubble oxygenators were used, but today only membrane oxygenators are in use. The membrane oxygenator is a coated bundle of hollow microporous polypropylene fibers tightly wound to create a large surface area. Blood flows around the tightly packed fibers and gas flows through the fibers. The gas, consisting of oxygen or a mixture of oxygen and medical-grade air, diffuses passively across the membrane and into the blood. The oxygen level in the blood can be controlled by changing the Fio₂. The amount of CO₂ removed from the blood is controlled by changing the liter gas flow rate or “sweep” of gas through the oxygenator. Volatile anesthetic can also be added to the fresh gas inlet that enters the oxygenator.

Heat Exchanger

The blood enters a heat exchanger either separately or in combination with the oxygenator (Figure 24-8 [2]). The heat exchanger is usually made of stainless steel tubes with heated or cooled water flowing through them. Blood flows around the tubes and the temperature is adjusted to the desired level. Traditionally patients were cooled in an effort to protect the heart and other vital organs during CPB. Today, active cooling is less common. Instead the patient’s temperature is allowed to naturally drop or drift while the surgery is performed. The patient is then actively rewarmed in preparation for the termination of CPB.

For some procedures, the patient is actively cooled to decrease the metabolic rate. This process is discussed later in the chapter under the heading “Surgery on the Ascending Aorta and Aortic Arch.” As the patient is rewarmed, gas solubility decreases, and it is possible for air bubbles to form in the CPB circuit. Consequently, the oxygenated blood passes through a filter before it is returned to the patient.

Arterial Filter

Finally, the blood passes through an arterial filter before returning to the arterial cannula and the rest of the body (Figure 24-8 [6]). The arterial filter has a pore size of 21 to 40 µm and acts as an air bubble trap and particulate filter preventing thrombi, fat globules, calcium, and tissue debris from entering the circulation. The arterial cannula is most often placed in the ascending aorta, but alternate sites include the femoral or the subclavian artery.

Accessory Pumps and Devices

Cardiotomy and Basket Suction: As illustrated in Figure 24-8, the perfusionist also operates several accessory roller pumps (generally located to the right of the main pump), used to control suction devices and deliver cardioplegia. An assistant helps improve the surgeon’s view by aspirating blood from the surgical field using a Yankauer or other suction tip. A “basket” type suction device can be placed in an open cardiac cavity to help drain the blood (Figure 24-8 [8]). This shed blood can then be returned to the patient in one of two ways. First, the blood can be returned to a portion of the venous reservoir known as the cardiotomy. The cardiotomy portion of the venous reservoir has a separate integrated filter that defoams the blood and removes air and debris that is picked up by the suction tip (pump sucker) used in the surgical field. Blood returned via the suction may contain fat, bone, and other debris. For that reason some surgeons prefer to return this blood to a separate cell-saver reservoir. Cell-saver blood is later centrifuged, washed, and returned to the patient. Research shows that systemic inflammatory markers decrease when shed blood is not returned to the patient undergoing CABG on CPB.^34,35 Using a cell-saver device instead of returning blood to the venous reservoir reduces the inflammatory response.³⁶ The disadvantage of this approach is that the volume of blood in the pump is reduced, especially if there is significant bleeding. If bleeding is a problem, the cell-saver blood can be washed and returned to the venous reservoir.

Left Ventricular Vent: The LV vent is a catheter placed in the left ventricle through the right superior pulmonary vein for the purpose of draining blood that accumulated in the cavity (Figure 24-8 [9]). Although blood is diverted from the heart during CPB, over time blood enters the LV from the bronchial arteries (which arise directly from the aorta or the intercostal arteries) or Thebesian vessels (coronary veins that drain directly into the heart). Blood and cardioplegia can also fill the LV if the patient has aortic insufficiency. This volume can cause the LV to distend, raise LVEDP, and compromise preservation by opposing the cardioplegia flow into the coronary arteries. Prior to inserting the vent, it is placed in a bowl of water to confirm that it is suctioning rather than blowing because accidental blowing of the vent could lead to an air embolism The vented blood returns to the cardiotomy.

Cardioplegia Pump: The perfusionist controls the infusion of cardioplegia by means of an accessory roller pump (Figure 24-8 [10]). A separate heat exchanger allows the temperature, as well as rate and pressure, to be controlled. Cardioplegia is discussed further in the section on myocardial preservation.

Anticoagulation

Systemic anticoagulation is always essential prior to cannulation and initiation of CPB. Without anticoagulation, clots can form in the pump that can lead to serious neurologic injury or death. Heparin, derived from porcine intestinal mucosa or bovine lung, is the preferred anticoagulant for cardiac surgery. It is a mucopolysaccharide that potentiates circulating antithrombin (AT III). It binds to AT III and increases its inhibitory action on the procoagulant effect of thrombin by 1000-fold. Heparin increases the speed of the reaction between AT III and multiple clotting factors including II, IX, X, XI, XII, and XIII. The standard cardiac dosage is 300 to 400 units/kg, administered preferably through a central intravenous line. Adequate anticoagulation is measured most commonly with point-of-care testing that includes activated clotting times (ACT) or heparin concentration assays (Hepcon). A baseline ACT is obtained sometime prior to heparin administration. The normal value is approximately 80 to 120 seconds. The ACT is measured 3 to 5 minutes after heparin administration. An ACT of more than 400 seconds (or more than 480 seconds, in some centers) is necessary before CPB is initiated. The lower limit ACT of 400 was determined in 1978 using monkeys on CPB. This level prevented the appearance of fibrin monomers in the CPB circuit.³⁷ A heparin concentration monitor (Hepcon) can be used in place of, or in addition to, the ACT measure. The Hepcon generates a heparin dose response (HDR) curve that can then be used to calculate the most appropriate dose of heparin to initiate CPB and maintain an adequate anticoagulation level during bypass. The amount of protamine needed to reverse the heparin after bypass is also calculated. The level of anticoagulation should be checked every 20 to 30 minutes during bypass so that more heparin can be given as needed to maintain a safe level of anticoagulation.

Patients who have been recently exposed to heparin may become “heparin resistant” and require higher doses of heparin to obtain therapeutic anticoagulation. Heparin resistance is defined as an ACT of less than 380 seconds despite administration of 400 units/kg of intravenous heparin.⁹ ATT III deficiency should be suspected if the patient does not become anticoagulated with additional heparin administration. ATT III deficiency can be treated empirically with 2 units of fresh frozen plasma, AT III concentrate, or recombinant AT III (rh AT III). Recombinant AT III has been shown to be effective in reducing heparin resistance by increasing circulating AT III without exposing patients to FFP.³⁸

Heparin-induced thrombocytopenia (HIT) is an immune reaction that occurs as a direct consequence of exposure to heparin. A comprehensive review of this disorder is found in Chapter 34. The 14C-serotonin release assay (SRA) and an enzyme-linked immunosorbent assay (ELISA) that detects antibodies to the platelet factor 4 (PF4) are used to definitively diagnose the disorder. For patients with a history of HIT, but a negative HIT antibody screen at the time of cardiac surgery, the American College of Chest Surgeons guidelines recommend the use of heparin only during CPB. There is a decreased risk of a patient being rediagnosed with HIT if the prior diagnosis of HIT was greater than 100 days before the scheduled cardiac surgery. Use of an anticoagulant other than heparin is recommended in the preoperative and postoperative period. In all cases, there should be no heparin added to the flush solution or heparin lock intravenous ports, and heparin-bonded catheters are avoided. Surgery should be postponed if feasible in patients with acute HIT and those who are antibody positive (subacute HIT). If urgent surgery is required, an alternative thrombin inhibitor such as bivalirudin or lepirudin is preferred. A secondary alternative is to block platelet activation using aspirin and an antiplatelet drug such as epoprostenol or tirofiban, and then proceed with heparin administration intraoperatively. ³⁹

Myocardial Preservation

Mild to moderate systemic hypothermia and cold cardioplegia are used for myocardial preservation. The patient can be actively cooled by the CPB circuit or his or her temperature can be allowed to drift toward the ambient room temperature. Some surgeons cool the heart topically by packing icy slush around it. The goal is to achieve hypothermic diastolic circulatory arrest to decrease the metabolic rate, oxygen consumption, excitatory neurotransmitter release, and to preserve high-energy phosphate substrates.⁹ The brain also benefits from the hypothermia and may be at least partially shielded from neurologic injury as a result. The cerebral metabolic rate decreases 6% to 7% for every degree Celsius decrease in brain temperature.

A hyperkalemic crystalloid solution mixed with blood is the most commonly used cardioplegia solution today. The ratio of the mix varies, but is most often a 4:1 blood to crystalloid solution. The exact composition in the mixture of cardioplegia solution is variable, but the first dose (induction dose) is cold (2° C to 5° C) with 20 to 30 mEq/L of potassium. Maintenance doses are also cold and contain 12 to 16 mEq/L of potassium. The goal is to maintain myocardial temperature between 8° C and 10° C.⁴⁰ Just before releasing the aortic cross-clamp, many surgeons administer a single terminal dose of warm blood (37° C) cardioplegia (TWBC). This so-called “hotshot” contains metabolic substrates (i.e., glucose, glutamine, and aspartate), which have been found to accelerate myocardial recovery from global ischemia.⁴¹ The amount of cardioplegia given in any single dose can be based on time, volume, or myocardial temperature according to the surgeon’s preference. It is generally redosed every 15 to 20 minutes while the aorta is clamped. ECG activity and/or an increase in myocardial temperature indicate that cardioplegia may need to be redosed sooner.

There are two possible approaches to delivering cardioplegia: antegrade, that is, down the coronary arteries; or retrograde, via the coronary sinus and cardiac veins. The first dose of cardioplegia is usually antegrade, and it is given just after placement of the aortic clamp. A catheter is inserted into the aortic root, just proximal to the aortic clamp, and cardioplegia is administered into the root and flows antegrade down the coronary arteries. Hypothermic diastolic circulatory arrest usually follows in 1 to 2 minutes depending on how well the heart is perfused. Antegrade cardioplegia can also be given directly down the coronary ostia when the aorta is opened for surgeries that involve the aorta or aortic valve. In CABG surgery, it is also infused directly into the new vein or arterial bypass grafts once the distal anastomosis is completed. Maintenance cardioplegia is administered every 15 minutes so the heart remains asystolic. Myocardial preservation is occasionally incomplete because the cardioplegia does not reach the entire myocardium either because the coronaries are blocked by atherosclerotic disease or because the solution has leaked into the left ventricle because of an incompetent aortic valve. When myocardial preservation is inadequate, there may be difficulty achieving diastolic arrest and electrical activity may reappear on the electrocardiogram (ECG) between doses of cardioplegia. Additionally, the fluid that leaks into the left ventricle when the patient has AI can cause the ventricle to distend. The increased pressure caused by the distension opposes the antegrade flow of the cardioplegia in the coronaries, thereby increasing the risk of myocardial ischemia. The purpose of the left ventricle vent is to suction out this fluid and prevent distension. In these cases, retrograde cardioplegia can significantly improve myocardial preservation. In fact, many surgeons choose to maximize myocardial protection by routinely giving both antegrade and retrograde cardioplegia.

In the retrograde approach, a catheter is blindly inserted into the right atrium and advanced into the coronary sinus, the largest venous drainage vessel of the heart. To place the catheter, the surgeon often lifts the heart to help locate the sinus and advance the catheter. If this catheter is placed before CPB, lifting and manipulation of the heart frequently results in dysrhythmias and hypotension. It is not unusual for this maneuver to cause atrial fibrillation (AF). Synchronized cardioversion of the AF may be required if the patient becomes hemodynamically unstable. Once the catheter is in place, cardioplegia is administered to the myocardium in a retrograde fashion through the cardiac veins. Retrograde perfusion protects the myocardium that is distal to the coronary obstructions.

Blood Conservation

According to the Society of Thoracic Surgeons (STS) database, 50% of cardiac surgical patients receive a blood transfusion.⁴² Currently 10% to 15% of the nation’s blood supply is used for patients having cardiac surgery. The risks of transfusion are well documented (see Chapter 20), and blood transfusions during cardiac surgery are associated with worse short-term and long-term survival.43,44 Additionally, the donor blood supply is either stable or decreasing.^45,46 Blood is considered a finite, scarce, and expensive resource, and there is a national effort to limit its use. Three preoperative risk factors have been linked to bleeding and blood transfusion: (1) advanced age (70 years or older); (2) low red cell volume either from preoperative anemia and/or small body size; and (3) urgent or complex surgery involving prolonged CPB times.⁴⁷

In 2011 the STS and the Society of Cardiovascular Anesthesiologists (SCA) published instructions for blood conservation in clinical practice guidelines.⁴⁷ Practitioners of cardiac anesthesia are encouraged to review this important document; this chapter discusses only the highlights. The recommended techniques that promote the conservation of blood and blood products include the administration of antifibrinolytics, blood salvage, limiting the quantity of pump prime, ultrafiltration when appropriate, and the development of multidisciplinary blood management teams.

Antifibrinolytics

Antifibrinolytics are commonly administered to cardiac surgical patients requiring CPB. Use of antifibrinolytics reduces surgical bleeding and decreases the incidence of blood transfusion.⁴⁷ Aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron) are both lysine analogs that inhibit plasmin, the key enzyme in the fibrinolytic cascade. Both drugs form a reversible complex with plasmin that then inhibits fibrinolysis or the natural breakdown of clot. Dosing regimens vary, but a common recommendation for aminocaproic acid is a 50 mg/kg bolus over 20 to 30 minutes followed by an infusion of 25 mg/kg/hr into the immediate postoperative period. A standard dosing regimen of tranexamic acid is 10 mg/kg over 20 minutes followed by 1 to 2 mg/kg/hr maintenance infusion into the immediate postoperative period. Dosing regimens vary among institutions. Tranexamic acid is known to be 5 to 10 times more potent than aminocaproic acid, but also more expensive. The use of aprotinin, a kallikrein inhibitor, was suspended in the United States in 2007 after an increase in mortality was noted in comparison to the other antifibrinolytics in the Blood Conservation Using Antifibrinolytics in a Randomized Trial (BART).⁴⁸