Chapter 10. Cardiac Anesthesia

The cardiac anesthesiologist is challenged with the requirements of maintaining general anesthesia while also serving as the patient's intensivist and diagnostician, facilitating the surgery and maintaining vital organ function. The objectives of a general anesthetic are analgesia, amnesia, and unconsciousness while supporting vital physiologic function and creating satisfactory operating conditions. An effective general anesthetic blunts the physiologic responses to surgical trauma and hemodynamic perturbations while permitting recovery at a predictable time after the operation. To accomplish this, the anesthesiologist must act as the patient's medical intensivist: support life with mechanical ventilation; control the circulation; and diagnose and treat acute emergencies that may occur during surgical incision, rapid changes in body temperature, extracorporeal circulation, and acute shifts in intravascular volume. The cardiac anesthesiologist must provide complex diagnostics in order to facilitate surgery by determining the competency of heart reconstructive procedures and measuring the cardiovascular response to altered cardiac anatomy and physiology. The task in cardiac surgery is unique because of the nature of the operations and the narrow tolerance for hemodynamic alterations in patients with critical cardiac disease. Anesthetic management of the cardiac surgical patient is intimately related to the planned operative procedure and the anticipated timing of intraoperative events.

The preoperative visit by the anesthesiologist is aimed at the formulation of an anesthetic plan based on the patient's surgical illness, scheduled operation, and concomitant medical problems. The medical history is elicited by questioning the patient and reviewing the medical records. The anesthesiologist must know the status of the cardiovascular system, related morbidity, and concurrent medications to design the anesthetic safely for a patient undergoing heart surgery. All anesthetic drugs have a direct effect on cardiac function, vascular tone, and/or the autonomic nervous system. The American Society of Anesthesiologists (ASA) has developed a physical status classification as a general measure of the patient's severity of illness (Table 10-1).1

In addition to contributing to postoperative morbidity, concurrent medical illness often defines an acceptable range for monitored parameters that are controlled during cardiac surgery. Acceptable intraoperative blood pressure may be altered based on several preoperative findings. The brain of a patient with long-standing severe hypertension may perfuse inadequately if the blood pressure during surgery is maintained only within what is typically considered a “normal” range because of a “rightward shift” of the cerebral autoregulation curve over time. History of a previous stroke often suggests intrinsic cerebrovascular disease that also may dictate alteration of blood pressure and blood product administration management. The response to bronchodilators in patients with chronic obstructive pulmonary disease may permit guided management of perioperative bronchospasm to ensure adequate respiration. A history of a difficult intubation or an adverse response to a specific drug is also highly relevant to the anesthesia plan.

Although a focused medical history pertaining to the patient's cardiac disease often takes priority, there are additional items in the history that are important to the cardiac anesthesiologist that might not be as pertinent in the realm of noncardiac surgery. For example, the presence of esophageal pathology could contraindicate the placement of a transesophageal echocardiography (TEE) probe (Table 10-2). A history of previous venous thrombosis or pulmonary embolism might make one consider avoiding anti-fibrinolytic medications. The presence of Reynaud's disease may complicate radial arterial catheterization.

The anesthesiologist is responsible for informing the patient of the conduct of the planned anesthetic and associated risks while obtaining consent for the anesthesia and related procedures. The exchange of information between patient and physician is often a balance between providing sufficient insight regarding possible complications without producing harmful anxiety. An outline of upcoming events accompanied by an informative discussion of risks and options typically leads to informed consent.

The preoperative ordering of tests evaluating cardiac function before noncardiac surgery, such as stress testing, echocardiography, and cardiac catheterization, are the focus of much debate and have generated an extensive literature.3,4 However, in cardiac surgery, these tests are part of routine cardiac surgical evaluation for operative planning. Although the decision to order these preoperative tests is not applicable to the cardiac anesthesiologist, the importance of their review is critical. Not only are these tests used in formulating an anesthetic plan but are also used to focus the intraoperative TEE examinations and as a basis for comparison to the operative TEE findings.

Laboratory tests are ordered to complement findings of the medical history and physical examination. Routine preoperative laboratory tests include a complete blood with platelet count; electrolyte battery with blood glucose, serum creatinine, and blood urea nitrogen levels; and prothrombin time and partial thromboplastin times. Other laboratory tests may be ordered based on patient-specific disease. A chest radiograph, electrocardiogram (ECG), and urinalysis complete routine testing. Pulmonary function tests are not routinely ordered and their usefulness in cardiac surgery is debatable except in lung transplantation. Outside of lung resection during thoracic surgery, they have not been found to be predictive of postoperative pulmonary complications.5,6 The review of chest computed axial tomography (CT) scans may have important implications for the cardiac anesthesiologist in patients with aortic disease such as aortic aneurysmal compression of the esophagus or major branches of the pulmonary arterial and main bronchial trees.

Most concurrent medications are continued until right up to the operation, including most cardiovascular medications. Oral medications can be taken according to schedule on the day of surgery with a small sip of water. Although increase in mortality after acute beta-blocker withdrawal have been more clearly shown in vascular surgery7,8 than in cardiac surgery, withdrawal in cardiac surgery has been linked to an increased incidence of postoperative supraventricular arrhythmias.9,10 Concern also exists with the preoperative discontinuation of vasodilators leading to perioperative vasoconstriction. The preoperative continuation of ACE inhibitors remains controversial given reports of postanesthesia induction hypotension and decreased perioperative renal perfusion.11–14 Although from a retrospective observational cohort study, its preoperative continuation has also recently been linked to an increased incidence of mortality, renal failure, and the necessity of inotropic support after cardiac surgery.15 For patients scheduled for late afternoon surgery and not receiving maintenance intravenous fluids, preoperative diuretics may be withheld to avoid preoperative dehydration. Finally, a potential for acute withdrawal must be considered after sudden cessation of chronic opioid or benzodiazepines use.

In contrast to antihypertensives, most anticoagulants are discontinued before surgery. Warfarin is generally stopped 5 days before the operation. In patients with mechanical heart valves, heparin bridge therapy is utilized. The oral anti-platelet drug, clopidogrel, is typically stopped for at least 5 days in order to allow the generation of new functioning platelets. When intravenous heparin is administered for unstable angina pectoris, it may be unwise to discontinue it preoperatively.

The physical examination includes measurement of height, weight, and vital signs as well as a comprehensive assessment of the heart, lungs, peripheral vasculature, and nervous system. The exam is often focused in order to quickly identify signs suggestive of circulatory deficiency, such as the lack of equal and bilateral pulses, lower extremity edema, ascites, distended neck veins, or the inability to lie flat. No anesthesiologist's exam is complete without a thorough examination of the airway. Samsoon's modification of the Mallampati classification used to predict a difficult airway is based on the examiner's ability to view intraoral structures:16,17

• Class 1: Soft palate, tonsillar fauces, tonsillar pillars, and uvula
• Class 2: Soft palate, tonsillar fauces, and uvula
• Class 3: Soft palate and base of uvula
• Class 4: Soft palate not visualized

Classes 1 and 2 represent airway anatomy associated with minimal difficulty with tracheal intubation. Classes 3 and 4 are more likely associated with an inability to intubate the trachea using conventional direct laryngoscopy. Other features associated with difficult intubations include a recessed chin, small mouth, large tongue, and inability to sublux the mandible.

Before the patient enters the operating room, the anesthesiologist formulates a plan to control the circulatory response to anesthesia, secure the airway, and maintain body homeostasis. Emergency operations are incompatible with leisurely preparation but instead are dictated by a sense of urgency. Rarely, however, is there any opportunity to provide reassurance to the patient or to prepare for the anesthetic and operation meticulously. The multidisciplinary nature of cardiac surgery requires precise communication between the anesthesiologist and the surgeon. Frank and open communication between all members of the operative team has been identified as an important element in the current effort to promote patient safety.

Extensive physiologic monitoring is employed during cardiac operations because virtually every major physiologic system required for life is affected. The reasons for physiologic monitoring are (1) to ensure patient safety in the absence of protective reflexes made ineffective by anesthetic drugs, (2) to enable pharmacologic and mechanical control of vital function, and (3) to diagnose acute emergencies that require immediate treatment. For example, morbidity as a consequence of breathing circuit disconnects, loss of oxygen from the hospital's central supply, or unrecognized esophageal or main stem endotracheal intubations can be prevented by capnography, pulse oximetry, airway pressure monitors, oxygen analyzers, and a stethoscope.

The senses of touch, hearing, and sight are the basic monitors. Electronic monitors are vigilance aids that supplement the anesthesiologist's perceptions. The selection of monitors is dictated by the utility of the data generated, expense, and risk. Routine or essential monitors that have been deemed cost-effective with low risk:benefit ratios include pulse oximetry, noninvasive blood pressure, capnography, temperature, ECG, precordial or esophageal stethoscope, and oxygen analyzers. These have been defined by the American Society of Anesthesiologists (House of Delegates, 1989) as essential monitors to be used in all surgical patients requiring anesthesia unless there are contraindications (eg, esophageal stethoscope during esophageal surgery) (Table 10-3). Other noninvasive and invasive monitors are used only with clear indication.

The growth in monitoring technology and sophistication is paralleled by an equal growth in cost. The balance between cost and enhancement of patient safety must be considered when additional monitoring is selected. It is difficult to justify a monitor that provides data that does not influence medical or surgical management.

Measurement of Blood Pressure

Blood pressure is the most commonly measured index of cardiovascular stability in the perioperative period. Anesthetics and surgery cause changes in blood pressure that are often rapid and may be great enough to cause harm unless anticipated and treated. However, a change in blood pressure that alters perfusion pressure may not change organ blood flow. This is because most vital organs can autoregulate blood flow in response to changes in mean arterial blood pressure, permitting constant blood flow over a range of perfusion pressures.18 In chronically hypertensive patients, the boundaries for autoregulation are shifted so that significant decreases in organ perfusion may occur with blood pressures in the considered “normal” range. Both the type and dose of anesthetic medications can affect the relationship between vital organ perfusion and blood pressure. For example, volatile anesthetics are potent vasodilators that tend to disrupt cerebral autoregulation in a dose-dependent manner to render blood flow more linearly dependent on blood pressure (Fig. 10-1).

Although noninvasive blood pressure monitoring suffices for most patients during routine noncardiac surgery, direct measure of arterial blood pressure with an indwelling arterial catheter is necessary for cardiac surgery in order to detect changes quickly, to measure nonpulsatile blood pressure during cardiopulmonary bypass, and to facilitate arterial blood sampling for laboratory analysis. The measuring system includes an intra-arterial catheter and low-compliance saline-filled tubing connected to a transducer with a pressure-sensing diaphragm. The transducer has a strain gauge that converts the mechanical energy (displacement of the diaphragm by a change in pressure) into an electric signal that typically is displayed as a pressure waveform with numeric outputs for systolic, diastolic, and mean pressures. The mean blood pressure is determined by calculating the area under several pulse waveforms and averaging over time. This represents a more accurate measure of mean arterial blood pressure than weighted averages of systolic and diastolic pressures.

The transducer requires a zero reference at the level of the right atrium. Any movement of the patient or the transducer that changes the vertical distance between the transducer and the right atrium affects the value of the blood pressure measured. If the transducer is lowered, the pressure diaphragm senses arterial blood pressure plus hydrostatic pressure generated from the vertical column of fluid contained in the tubing and displays a falsely high blood pressure. A transducer elevated above the zero reference level decreases the displayed blood pressure. A 1-cm column of water (blood) exerts a hydrostatic pressure equal to 0.74 mm Hg. Small changes in patient or transducer position have a relatively insignificant effect on arterial blood pressure measurements but have a more important effect on lower-amplitude pressure measurements, such as central venous, pulmonary artery, and pulmonary artery occlusion pressures.

The radial artery is the most common site for insertion of an intra-arterial catheter. Twenty-gauge catheters are preferred when the radial artery is used because larger catheters are more likely to cause thrombosis. The wrist is chosen for arterial cannulation most often because of dual blood supply to the hand, preventing ischemia in the setting of a catheter related thrombosis. A patent palmar arch allows the hand to remain perfused despite a potential thrombosis of either the radial or ulnar artery assuming adequate flow through the other vessel. Distal embolization remains a risk though. The radial is the more superficial vessel and generally considered easier to cannulate. The Allen's test was designed to assess ulnar and palmar arch blood flow during abrupt occlusion of the radial artery, but its value to predict morbidity with radial artery cannulation is equivocal.19 Other sites selected for the insertion of an intra-arterial catheterization include the brachial, axillary, and femoral arteries.

The contour of the arterial pressure waveform is different in central and peripheral arteries. The propagating pressure waveform loses energy and momentum with a corresponding delay in transmission, loss of high-frequency components such as anacrotic and dicrotic notches, lower systolic and pulse pressures, and decreased mean pressure.20 The changes in the pulse waveform can be attributed to damping, blood viscosity, vessel diameter, vessel elastance, and the effects of reflectance of the incident arterial waveform by the artery-arteriolar junction.21,22 The blood pressure waveform measured in the ascending aorta is minimally affected by reflected waves in contrast to measurement of blood pressure in the dorsalis pedis or radial artery.

The contour of the pressure waveform can also be affected by the physical construction of the monitoring system. A hyper-resonant response to a change in pressure, or ringing, occurs when the frequency response of the monitoring system (ie, extension tubing, catheter, and stopcocks) is close to the frequency of the pressure waveform.20 The natural or resonant frequency fn of a monitoring system is defined by

where C is compliance of the measuring system, L is the length of the tubing, D is the diameter of the catheter extension tubing, and p is the density of the solution.

To prevent ringing, the natural frequency of the monitoring system fn must be greater than the frequencies of the pulse waveform. Any process that decreases fn, such as narrow, long, compliant tubing, may cause ringing.23 Ringing increases the value of the systolic blood pressure and decreases the value of the diastolic blood pressure but generally does not affect the value of the mean arterial pressure.

Damping is the tendency of the measuring system, through frictional losses, to blunt the peaks and troughs in a signal.24 Kinks in the pressure tubing or catheter, stopcocks, and air bubbles contribute to damping. Overdamped systems underestimate systolic blood pressure and overestimate diastolic blood pressure. When long lengths of tubing are necessary, deliberate damping may improve the fidelity of the arterial waveform.

Testing a measuring system for ringing and damping ensures that an arterial contour is reproduced faithfully. A simple test involves a brief flush of the high-pressure saline-filled catheter extension assembly. Flush and release should produce a rapid return of the pressure waveform to baseline with minimal oscillations. A gradual return to baseline and loss of higher-frequency components of the waveform suggests overdamping. A rapid return to baseline followed by sustained oscillations suggests ringing.

Electrocardiogram

The intraoperative ECG monitor has evolved from the fading-ball oscilloscope to a sophisticated microprocessor analog display. ECG signals are filtered digitally to eliminate electrical artifact produced by high-frequency (60-Hz) electrical power lines, electrocautery, patient movement, and baseline drift. The bandwidth filter modes are diagnostic, monitor, and filter. The diagnostic mode has the widest bandwidths (least filtered signal) and is preferred for detecting ST-segment changes caused by myocardial ischemia. Monitor and filter modes have progressively narrower bandwidths that effectively eliminate high-frequency interference and baseline drift but decrease the sensitivity of detecting ST-segment changes and decrease the specificity of ST-segment change to diagnose myocardial ischemia. Abnormal ST-segment depression (>1 mV) can occur from excessive low-frequency filtering and result in the misdiagnosis of myocardial ischemia. Filter modes are useful for detecting P waves and changes in cardiac rhythm in the presence of high-frequency interference.

The ECG is the most sensitive and practical monitor for the detection and diagnosis of disorders of cardiac rhythm and conduction and myocardial ischemia and infarction. Continuous monitoring of leads II and V5 is common (Fig. 10-2). Together these leads detect greater than 90% of ischemic episodes in patients with coronary artery disease who have noncardiac surgery.25

Diagnostic criteria for myocardial ischemia based on the ECG are (1) acute ST-segment depression greater than 0.1 mV 60 ms beyond the J point or (2) acute ST-segment elevation greater than 0.2 mV 60 ms beyond the J point26 (Fig. 10-3). The normal ST-segment curves smoothly into the T wave. Flat ST segments that form an acute angle with the T wave or downsloping ST segments are worrisome for subendocardial ischemia. ST-segment elevation occurs with transmural myocardial injury but also may occur after direct current (dc) cardioversion and in normal adults. The lack of specificity of ST-T-wave changes for myocardial ischemia is a major limitation of intraoperative ECG monitoring. Pericarditis, myocarditis, mitral valve prolapse, stroke, and digitalis therapy may produce changes in the ST segment that mimic myocardial ischemia.

Digital signal processing handles much larger quantities of information than the unaided eye and may increase the ability to detect ischemic episodes. ST-segment position analyzers automatically measure the displacement of the ST segment from a predetermined reference and enhance the ability to quantify changes in ST-segment position. Appropriate application requires accurate identification of the various loci in the P-QRS-T-wave complex. The operator defines the baseline and the J point of a reference QRS complex by movement of a cursor. New QRS-T-wave complexes are superimposed onto a predefined mean reference complex. Vertical ST-segment displacement is measured in millivolts and displayed graphically in 1-mV increments (Fig. 10-3). Because the accuracy of automated ST-segment monitoring is vulnerable to baseline drift and dependent on appropriate identification of the PR and ST segments, the diagnosis of myocardial ischemia is always verified by inspecting the actual ECG tracing.

Disturbances of rhythm and conduction are common during anesthesia and especially during cardiac surgery. Instrumentation of the heart, hypothermia, electrolyte abnormalities, myocardial reperfusion, myocardial ischemia, and mechanical factors such as surgical manipulation of the heart affect normal propagation of the cardiac action potential. Heart rate is measured by averaging several RR intervals of the ECG. The ECG may not sense the R wave of the selected lead if the electrical vector is isoelectric. A prominent T wave or pacemaker spike may be miscounted as an R wave by the ECG and artifactually double the rate. Usually, heart rate is best monitored by selecting the lead with an upright R wave and adjusting the sensitivity.

The QT interval can be measured only on hard copy. A normal QT interval is less than half the RR interval, but the QT interval must be corrected for heart rates higher than 90 or lower than 65 beats per minute. A prolonged QT interval increases the risk of reentrant ventricular tachydysrhythmias and may occur from hypokalemia, hypothermia, and drug effect (eg, quinidine or procainamide).

The ECG is monitored to confirm the electrical dormancy of the heart during aortic cross-clamping and perfusion with cold cardioplegia. Hypothermia decreases action potential conduction velocity, and high-dose potassium decreases the transcellular membrane potassium concentration gradient to prevent depolarization of cardiac muscle. During cardiopulmonary bypass and aortic cross-clamping, the loss and persistent absence of electromechanical activity suggest that myocardial oxygen consumption is maintained at a minimum.

Monitoring the ECG is most valuable when it begins before induction of general anesthesia. A hard copy of the pertinent leads permits comparison should a change be detected. An abnormal or marginal finding is less worrisome if it was present in the preoperative ECG and remains unchanged during the perioperative period. However, new-onset ST-T-wave changes or disturbances in rhythm and conduction suggest an ongoing active process that usually requires immediate attention.

Capnography

Capnometry is the measure of carbon dioxide (CO2) concentration in a gas. The capnogram is the continuous graphic display of airway carbon dioxide partial pressure (Fig. 10-4). The capnogram is the single most effective monitor for detecting esophageal intubation, apnea, breathing circuit disconnects, accidental extubation of the trachea, and airway obstruction. Tracheal intubation is verified by detection of physiologic carbon dioxide concentrations in the exhaled gas. Changes in its contour reflect disorders of ventilation, carbon dioxide production, or carbon dioxide transport to the lungs. A steep increase in the phase 3 slope of the exhaled CO2 concentration suggests partial airway obstruction, either mechanical (eg, tube kinking) or physiologic (eg, bronchospasm). A progressive decrease in exhaled carbon dioxide concentration occurs with decreased CO2 production (eg, hypothermia), increased minute ventilation, or increases in physiologic dead space ventilation such as pulmonary embolus or a drop in cardiac output. A progressive increase in exhaled carbon dioxide concentration occurs with hypoventilation, increased CO2 production (eg, malignant hyperthermia), or increased delivery of CO2 to the lungs (eg, during weaning off bypass with an increase in pulmonary blood flow). Despite the complex interplay of mechanical and physiologic factors that affect the shape of the capnogram, with any abrupt change in contour, an acute change in the patient's cardiovascular, pulmonary, or metabolic state should be considered.

Anesthetic Gas Monitors

Inhaled volatile anesthetics are different from other parenteral medications. They are delivered as a vapor through the breathing circuit. The clinical effect is determined by the partial pressure of this vapor in the brain, which is in equilibrium with the blood and the alveoli. Measuring the partial pressure of the volatile anesthetic at end expiration approximates the partial pressure in the alveoli and therefore the brain. Monitoring the end-tidal gas mixture adds precision to the administration of inhaled anesthetics and guards against inadvertent overdose.

The concentration of anesthetic gases is displayed as a percentage of the partial pressure of the anesthetic vapor to atmospheric pressure. This concentration can be measured using a variety of techniques, including mass spectroscopy, infrared spectroscopy, Raman spectroscopy, electrochemical and polarographic sensors, and piezoelectric absorption.27

Pulse Oximetry

Pulse oximeters were adopted universally into the practice of anesthesia almost immediately after their introduction despite the lack of published data demonstrating improved outcome with their use. The pulse oximeter is reusable, inexpensive, and noninvasive while providing continuous online data regarding the arterial hemoglobin saturation and pulse rate. The pulse oximeter can detect a decrease in oxyhemoglobin saturation even before changes in the color of the patient's skin or blood are evident.28 Its major limitations include a subjectivity to electrical interference and motion artifact as well as a high failure rate during periods of low flow or inadequate perfusion. In addition, pulsatile flow is required for proper function.29

The pulse oximeter is able to measure the percentage of oxyhemoglobin in arterial blood because of differences in the optical absorption properties of oxy- and deoxyhemoglobin. Using transillumination, oximetry emits wavelengths of 660 and 940 nanometers (nm). Oxyhemoglobin has a higher optical absorption in the infrared spectrum (940 nm), whereas reduced hemoglobin absorbs more light in the red band (660 nm). The ratio R of light absorbance at the two wavelengths is a function of the relative proportions of the two forms of hemoglobin. Rapid signal processing then permits reliable and rapid determination of the relative proportion of oxy- and deoxyhemoglobin. Calculation of arterial hemoglobin saturation is based on calibration algorithms derived from R ratios in healthy volunteers.

Arterial oxyhemoglobin saturation is distinguished from venous through the use of photoplethysmography by isolating the pulsatile component of the absorbed signal. The peaks and troughs in the blood volume pulse of the site being transilluminated produces a corresponding pulsatile effect on light absorption, rendering the calculated oxyhemoglobin saturation independent of nonpulsatile venous blood and soft tissue. Because the R values were determined in healthy volunteers, they are less accurate at oxyhemoglobin saturations below 70%. Motion artifact produces a high absorption of light at both wavelengths and an R value of approximately 1, which corresponds to an oxyhemoglobin saturation of approximately 85%.

Measurement of Temperature

Profound changes in body temperature during cardiac surgery are common, often deliberate, and affect vital organ function (Fig. 10-5). Anesthetized patients are poikilothermic. Intrinsic temperature regulation normally controlled by the hypothalamus fails during general anesthesia. Hypothermia occurs by passive and active heat loss. Passive mechanisms of cooling include radiation, evaporation, convection, and conduction. Active cooling usually occurs with extracorporeal circulation and with the use of cold or iced solutions poured into the chest cavity. Deliberate hypothermia during cardiac surgery is designed to arrest and cool the heart, decrease systemic oxygen consumption, and protect organs from hypoperfusion. Hyperthermia may result from preexisting fever, bacteremia, malignant hyperthermia, or overzealous rewarming during cardiopulmonary bypass. The monitoring and control of systemic temperature is important because either unintentional hypothermia or hyperthermia can be deleterious to the patient.

Hypothermia after cardiopulmonary bypass is the result of ineffective or most commonly insufficient rewarming. Cold operating rooms; cold, wet surgical drapes; a large surgical incision; and administration of cold intravenous fluids also contribute. Hypothermia exacerbates dysrhythmias and coagulopathy, potentiates the effects of anesthetic drugs and neuromuscular blockers, increases vascular resistance, decreases the availability of oxygen, and contributes to postoperative shivering. The elderly are especially susceptible because of limited compensatory reserve. Although there is evidence to support the efficacy of mild therapeutic hypothermia for brain protection after cardiac arrest and subsequent resuscitation,30 the optimal target temperature of induced hypothermia for neuro-protection during cardiopulmonary bypass, or even the need for hypothermia at all remains highly contentious in cardiac surgery currently.31,32

Temperature typically is monitored from several sites during cardiac surgery. Blood temperature can be measured from the tip of a pulmonary artery catheter and within the cardiopulmonary bypass circuit (typically venous and arterial lines). Blood temperature is the first to change in response to deliberate hypothermia or active rewarming during cardiopulmonary bypass. Nasopharyngeal and tympanic temperatures reflect the temperature of the brain and closely track blood temperature because these sites are highly perfused. Rectal and bladder temperatures provide a measure of core temperature only at equilibrium. Esophageal temperature often underestimates core temperature because of the cooling effects of ventilation in the adjacent trachea. Axillary and inguinal temperatures are shell measurements and are impractical. The possibility of an increased gradient between the measured nasopharyngeal and actual brain temperature should be considered and careful attention should be made to prevent cerebral hyperthermia.33 Arterial inflow temperatures during rewarming should be limited to a maximum of 37 to 37.5°C to help prevent a large gradient between the inflow temperature and the brain temperature. Post operative hyperthermia has been associated with a worsened neurologic outcome.33

The degree and site of temperature changes are important indicators of an intact circulatory system. A persistent discrepancy in temperature between two sites may be a sign of malperfusion. Rewarming during cardiopulmonary bypass normally is associated with an increase in nasopharyngeal or tympanic temperature accompanied by a more gradual increase in temperature in organs with low perfusion. A persistently cold nasopharynx with a normal rate of increase in rectal temperature may be a result of aortic dissection and hypoperfusion of the head.

Measurement of Cardiac Output and Central Venous and Pulmonary Artery Pressures

Cannulation of the central venous circulation permits central administration of drugs, rapid administration of fluids through short, large-bore cannulas, and the measure of central venous pressure. The most commonly used site for central venous access is the internal jugular vein because of reliable insertion, ease of access from the head of the table, decreased risk of pneumothorax, and decreased risk of catheter kinking during sternal retraction. The subclavian vein is the preferred site for insertion of a central venous catheter for long-term intravenous total parenteral nutrition because of a decreased risk of blood-borne infection.34 The most important complication of internal jugular vein cannulation is inadvertent puncture or cannulation of the carotid or subclavian artery. Cannulation of the central venous circulation is confirmed by manometry, either electrical or mechanical, before insertion of a large-bore catheter. Ultrasound-guided cannulation of the internal jugular vein renders the procedure less dependent on anatomic landmarks and is associated with a decrease in the number of unsuccessful cannulation attempts35 (Fig. 10-6). With the advent and wide availability of portable ultrasound imaging devices, ultrasound-guided central venous cannulation is becoming commonplace to increase the success rate and decrease the risk of complications.36 TEE can be used to verify the presence of a wire in the right atrium or superior vena cava (SVC). It can also be used to verify correct placement of the central venous or pulmonary artery catheter tip.37

Central venous pressure (CVP) can be measured via the central venous catheter or a proximal port in a Swan-Ganz catheter. The pressure is best measured at end exhalation to exclude the transmission of intrathoracic pressure. The CVP tracing is normally composed of five waves. The A and C waves represent atrial contraction and isovolumetric right ventricular contraction. The X descent occurs with right ventricle ejection as the tricuspid annulus descends. The V and Y waves represent right atrial filling, first during late ventricular contraction and then during early diastole with tricuspid valve opening.

The CVP is traditional thought of as a measure of the overall volume status of a patient, with normovolemia represented by a CVP of 6 to 10 mm Hg during positive pressure ventilation. However, studies have consistently shown that the CVP does not correlate with measured circulated blood volume or fluid challenge responsiveness.38–41 The CVP value is dependent on the interaction between cardiac function and venous return. Venous return can be affected not only by the mean circulatory filling pressure (the equalization of pressure throughout the entire vascular system if heart was theoretically stopped temporarily) and the cardiac function but also by changes in venous tone. For example, after the induction of general anesthesia, a drop in CVP often represents anesthetic induced venodilation, not acute hypovolemia. The sensitivity of the CVP as a measure of volume status is affected by the body's advanced compensatory mechanisms designed to maintain homeostasis, and these significant changes in blood volume may not be associated with a change in the CVP. A 10% loss of blood volume can easily be compensated for by an auto-transfusion of volume from venous capacitance vessels without a change in the CVP and significant volume loading can occur without a concomitant rise in CVP as fluid accumulates in the same splanchnic venous beds.

Using the CVP as a measure of volume status is further complicated by the differences between intramural and transmural pressure. The pressure measured by an intravascular catheter represents the intramural pressure. The transmural pressure is the difference between the intramural pressure and the pressure surrounding the vascular structures. This difference represents the driving pressure for venous return whereas the measured intramural pressure may not. Increases in intrathoracic and intra-abdominal pressure as well as pericardial pressure will be transmitted to the intravascular space, increasing the CVP without increasing transmural pressure and thus without increasing venous return or indicating a degree of hypervolemia.

Beyond simply measuring pressure, the contour of the CVP waveform can provide other important clinical information. The presence of cannon A waves can confirm the diagnosis of a junctional rhythm in situations wherein the ECG is difficult to discern (also seen with tricuspid stenosis or right ventricular diastolic dysfunction). Large V waves during ventricular systole occur with significant tricuspid regurgitation. Deep X and Y descents can be seen during right sided volume overload, often in conjunction with tricuspid regurgitation. Right ventricular diastolic dysfunction can be suggested by a flattening of the Y descent.

Pulmonary artery catheters (PAC) are inserted via the central venous circulation through the right side of the heart with the catheter tip positioned just downstream of the pulmonic valve. The PAC can measure pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output, and mixed venous oxygen saturation and also permits the calculation of the derived values of systemic and pulmonary vascular resistance. The pulmonary artery occlusion pressure can be used as an index of left ventricular preload in the absence of mitral stenosis. However, the use of this pressure measurement to estimate preload is limited because of variability in left ventricular size and compliance. Pulmonary artery occlusion pressures (PAOP) can be affected by myocardial compliance, mode of ventilation, and ventricular afterload. Similar to the CVP, the PAOP can also be affected by increases in intrathoracic, intra-abdominal, and pericardial pressure. Increases in PA pressures or PAOP may often indicate myocardial dysfunction or myocardial ischemia (Fig. 10-7). Hemodynamic parameters derived from the pulmonary artery catheter have been shown not to be as sensitive or as specific for detecting myocardial ischemia as the ECG.42

Complications associated with insertion of a PAC include infection, dislodgment of endocardial pacemaker wires, dislodgement of right atrial or ventricular clot or tumor, atrial and ventricular arrhythmias, pulmonary infarction, pulmonary artery rupture, perforation of the right atrium or ventricle, catheter entrapment, and heart block. The incidence of right bundle-branch block (RBBB) from catheter insertion is approximately 3% and may lead to complete heart block in patients with a preexisting left bundle-branch block (LBBB).43 Most PACs are now heparin-bonded to decrease the incidence of thrombus formation.44 Chronic indwelling PACs are associated with a progressive thrombocytopenia.45

Multiport pulmonary artery catheters equipped with a tip thermistor permit the measurement of pulmonary blood flow or cardiac output by thermodilution. Thermodilution cardiac output uses an indicator-dilution technique. The indicator, a known volume of cold saline, is injected rapidly into a proximal port in the right atrium. Cardiac output (CO) is calculated from the rate of change in blood temperature at the PAC catheter tip over time using the Stewart-Hamilton equation:46,47

where CO is cardiac output, V is the volume of the injectate, TB is the blood temperature at time 0, T1 is the injectate temperature at time 0, ΔTB(t) is the change in blood temperature at time t, K1 is the density factor, and K2 is the computation factor.

Thermodilution measures the degree of mixing that occurs between the cold injectate and blood. More mixing implies increased flow. Complete mixing of 10 mL of cold injectate with a circulating blood volume produces a small decrease in temperature at the catheter tip. Poor mixing, suggestive of slow, sluggish flow, produces a large decrease in temperature as the injectate bolus passes the thermistor. The derived value for cardiac output is inversely proportional to the area under the thermodilution curve. Rapid infusion of cold intravenous fluids at the time of measurement may falsely increase the derived cardiac output. Thermodilution measures right-sided cardiac output, which will not equal left-sided cardiac output in patients with intracardiac shunts.

Cardiac output may be monitored nearly continuously using a specialized PAC. The continuous cardiac output catheter intermittently heats blood adjacent to a proximal portion of the catheter and senses changes in blood temperature at the catheter tip using a fast-response thermistor. The method requires no manual injections, and values are acquired, averaged, and updated automatically every several minutes. The only true disadvantage to these catheters is the increased cost.

Mixed venous oxygen saturation (Sv̅O2) can be measured intermittently by manual blood sampling from the pulmonary artery port or continuously using a modified PAC equipped with an oximeter. Assuming normal oxygen consumption, a normal (Sv̅O2) generally denotes adequate oxygen delivery but does not provide information about the adequacy of perfusion to specific organs. A normal (Sv̅O2) may not reflect adequate tissue perfusion in patients with intracardiac shunts, sepsis, or liver failure. Oxygen consumption may change significantly during or after cardiac surgery as patients are warmed or as they begin to emerge from anesthesia, leading to a drop in (Sv̅O2). However, a significant decrease in (Sv̅O2) often signifies a decrement in oxygen delivery representing compromised cardiac output, anemia, or hypoxia.

Sv̅O2 provides an alternative method to calculate cardiac output if oxygen consumption is assumed based on a nomogram derived from resting awake subjects. By the Fick equation, cardiac output is equal to the rate of systemic oxygen consumption divided by the arterial-venous oxygen content difference:

where Vo2 is oxygen consumption, CO is cardiac output, Cao2 is the oxygen content in arterial blood, and CvO2 is the oxygen content in mixed venous blood. Errors may occur when oxygen consumption is well below the assumed nomogram in sedated, hypothermic, or anesthetized patients, with an overestimation of cardiac output.

Although routine use of a pulmonary artery catheter for monitoring patients during cardiac operation is debated, it does provide clinical information that is used to direct therapy in high-risk patients (Figs. 10-8 and 10-9). The pulmonary artery catheter appears to demonstrate continued utility in the care of patients with pulmonary hypertension and right ventricular dysfunction.48 Because an insidious decrease in (Sv̅O2) may be an early warning of impending circulatory insufficiency, ventricular dysfunction, ongoing bleeding, or impending tamponade, (Sv̅O2) pulmonary artery catheters may be particularly useful in the intensive care unit, where early deterioration can be detected and treated before an adverse event occurs.

Measurement of Electrolyte Concentration

Electrolyte abnormalities are common during and after cardiopulmonary bypass and are measured intermittently, typically using stat laboratory tests.49 The capability to detect and treat electrolyte disturbances is an important aspect of intraoperative care.

Abnormalities in sodium and water homeostasis are often associated with heart failure and compounded by hemodilution during surgery with or without cardiopulmonary bypass. Nonosmotic secretion of arginine vasopressin provoked by surgical stress, pain, hypotension, or nonpulsatile perfusion contributes to the development of hyponatremia by stimulating renal retention of free water. A 2- to 5-mEq/L decrease in the plasma sodium concentration is expected after beginning cardiopulmonary bypass but does not normally require treatment. Hypernatremia may be caused by excessive diuresis without free-water repletion or by the administration of hypertonic sodium bicarbonate solutions. An 8.4% sodium bicarbonate solution has an osmolality of 2000 mOsm/l or 6.9 times the osmolality of plasma. Hyperkalemia is common because of high-potassium cardioplegic solutions that are distributed into the systemic circulation. Hyperkalemia during cardiac surgery also may be caused by hemolysis, acidosis, massive depolarization of muscle, and tissue cell death. Increasing serum potassium concentration is manifested by peaked T waves, a widened QRS complex, disappearance of the P wave, heart block, and conduction abnormalities that may be life threatening. Very high concentrations of potassium used to provide cardioplegia inhibit spontaneous depolarization and produce asystole. Patients with diabetes mellitus are at increased risk for hyperkalemia because cellular uptake of potassium is mediated by insulin. Impaired renal excretion of potassium enhances hyperkalemia in patients with renal insufficiency. The initial treatment of hyperkalemia is aimed at redistributing extracellular potassium into cells, but the elimination of potassium from the body requires excretion by the kidneys or gastrointestinal tract. Insulin and glucose administration rapidly decrease extracellular potassium by redistributing the ion into cells. Alkalosis, hyperventilation, and beta-adrenergic agonists also favor redistribution of potassium into cells, but the response is less predictable. Calcium carbonate and calcium chloride antagonize the effects of hyperkalemia at the cell membrane. A typical intravenous dose of glucose and insulin for the acute treatment of hyperkalemia is 1 g/kg of glucose and 1 unit of regular insulin per 4 g of glucose administered.

Hypokalemia can occur during cardiac surgery from hemodilution with nonpotassium priming solutions, diuresis, or increased sympathetic tone during nonpulsatile perfusion. Intraoperative hypokalemia is exacerbated by preoperative potassium depletion from chronic diuretic therapy. Routine insulin administration for hyperglycemia and the frequent use of beta2-adrenergic agonists stimulate cellular uptake of potassium, also contributing to the frequent occurrence of hypokalemia in cardiac surgical patients. Hypokalemia predisposes to atrial arrhythmias, ventricular ectopy, digitalis toxicity, and prolonged response to neuromuscular blocking drugs. Hypokalemia is treated by slow administration of KCl in increments of 10 mEq, with potassium concentrations measured between doses.

Hypocalcemia decreases myocardial contractility and peripheral vascular tone and is associated with tachycardia.50,51 Hypocalcemia produces prolongation of the QT interval and T wave inversions, but significant arrhythmias owing to disturbances in ionized calcium concentration are not common. Hypocalcemia occurs soon after the onset of cardiopulmonary bypass but may resolve without treatment. Increasing serum concentrations of parathyroid hormone during cardiopulmonary bypass may explain, in part, the gradual increase in ionized calcium concentration to precardiopulmonary bypass levels.52 The etiology of cardiopulmonary bypass–induced hypocalcemia probably is multifactorial, but hemodilution and decreased metabolism of citrate after rapid blood transfusion are contributing factors. The routine administration of calcium salts without prior measurement of ionized calcium concentration poses the risk of hypercalcemia. Excessive calcium administration may increase the risk of postoperative pancreatitis and myocardial reperfusion injury.53

Magnesium deficiency is common in cardiac surgical patients, and acute magnesium supplementation decreases the incidence of postoperative cardiac dysrhythmias and overall morbidity after cardiac operations.54,55 However, measuring total plasma magnesium concentration has questionable clinical significance because the value primarily reflects the concentration of protein-bound magnesium and not physiologically active, ionized magnesium.56

Blood glucose control for cardiac surgery is controversial. Most would agree that treatment of severe hyperglycemia is warranted. Hyperglycemia has been shown to increase morbidity and mortality in nonsurgical patients after stroke and myocardial infarction as well as in patients after cardiac surgery.57–59 However, there are conflicting data regarding support for an aggressive treatment strategy designed at normalizing blood glucose. In a mixed surgical critical care population, intensive insulin therapy to maintain glucose ≤110 mg/dl reduced morbidity and mortality but with an increased incidence of hypoglycemia.60 In a meta-analysis of randomized clinical trials conducted in intensive care units, evidence suggested that intensive insulin therapy significantly increased the risk of hypoglycemia and offered no overall mortality benefit.61–63 Thus far, the literature has only focused on glucose control in the intensive care units. The benefit, if any, of glucose control during cardiac surgery currently remains unknown. No evidence exists supporting or refuting aggressive control. The stress of cardiac surgery, acute changes in catecholamine levels, large swings in body temperature, administration of steroids, and large volumes of intravenous fluids all affect blood glucose. The efficacy of intravenous insulin to reduce blood glucose is further complicated by hypothermia when insulin degradation is slowed as is insulin's ability to induce cells to increase glucose uptake (ie, insulin resistance). Over simplistic protocols that do not take into account the increased half life of intravenous insulin and its decreased effectiveness during cold conditions may result in patients receiving progressively increasing doses of insulin with little immediate effect. The slowly metabolized insulin will linger during hypothermia. With systemic rewarming, the large depots of insulin could produce severe hypoglycemia as well as clinically significant hypokalemia. Regardless of glucose management strategy, rapid and frequent measurement of blood glucose is essential.

Monitoring the Nervous System

Neurologic complications, including stroke, paralysis, cognitive dysfunction, blindness, and peripheral nerve injury, are second only to heart failure as the major cause of morbidity and mortality after cardiac surgery.64 Because a full neurologic examination is not possible during general anesthesia, the objective of intraoperative neurophysiologic monitoring is to provide a means for early detection of neurologic injury or impending injury to permit early intervention in an effort to restore function before the injury becomes permanent.

Electroencephalography (EEG)

EEG is a measure of spontaneous electrical brain activity recorded from electrodes placed in standard patterns on the scalp. Electrical activity of individual electrodes is amplified and then recorded as continuous wavelets that have different frequencies and amplitudes. These data can be displayed as raw EEG or broken down into basic components of frequency and amplitude and displayed as a spectral analysis. A change in EEG activity from baseline during a procedure may indicate ischemia of the cerebral cortex as a consequence of hypoperfusion. Intraoperative EEG can also detect seizure activity masked by general anesthetics or electrocortical silence induced by deliberate hypothermia.

Intraoperative application of EEG can be justified for any cardiac operation where there is a risk for cerebral hypoperfusion such as combined cardiac and carotid endarterectomy procedures. EEG is very sensitive for detecting cerebral malperfusion and can be used to detect malperfusion of the aortic arch branch vessels during aortic dissection repair.65 Hypothermia produces dose-dependent slowing of the EEG. The predictable actions of hypothermia on EEG activity have made EEG a useful monitor and surrogate for brain temperature in order to determine the adequacy of deliberate hypothermia for circulatory arrest procedures.66 When performing intraoperative EEG, it is important to recognize that anesthetic agents can attenuate EEG amplitude and frequencies. Marking the EEG in the event of bolus sedative hypnotic administration or when the inhaled anesthetic concentration is changed will help to distinguish EEG changes caused by general anesthetics from changes as a consequence of neurologic injury.

Bispectral Index

The occurrence of awareness under anesthesia is a rare, approximately 0.2% with general anesthesia.67 In patients at high risk for awareness, the incidence may be near 1%.68,69 Cardiac surgery is associated with an increased risk of intraoperative awareness.69–73 The American Society of Anesthesiologists published a “practice advisory” intended to assist decision making pertaining to this issue.74 The consequences of anesthetic awareness can be significant, leading to long-term psychologic distress including post-traumatic stress disorder. This is caused by several factors, such as hemodilution of intravenous anesthetics from the bypass circuit, hemodynamic instability leading to the decrease or discontinuation of anesthetics, and the inability to measure end-tidal concentrations of inhaled anesthetics if used during bypass. There are several devices commercially available for monitoring anesthetic depth. The bispectral index or BIS monitor (Aspect Medical Systems) is the most widely used of these devices. By using a pad placed directly on the scalp, a frontal electroencephalogram signal is processed in order to calculate a dimensionless value of the patient's level of consciousness. The BIS values range between 0 and 100 with below 40 indicating a deep level of consciousness and between 40 and 60 considered adequate for most general anesthetics.75 It's clinical utility in preventing anesthetic awareness or reducing over-administration of anesthetics has been studied in several randomized trials with mixed results.67,75,76

Near Infrared Cerebral Oximetry

Although the technology has been in existence for over 25 years,77 only within the last 5 to 10 years has the use of continuous noninvasive cerebral oxygen saturation monitoring expanded. The device is based, like pulse oximetry, on the different absorption characteristics of oxygenated and deoxygenated hemoglobin when exposed to near infrared spectrum light (NIRS). Applied on each temple are two pads that each emits a near-infrared light signal that penetrates all tissues in the cranium using the transillumination characteristics of the skull. Signal contamination from extracerebral tissue saturations such as the bone and soft tissue are prevented from mixing with those from the brain and cerebral vasculature by using the concept of spatial resolution. Each pad employs two separate signal detectors at predetermined distances from the original light source. Signals from shallow tissues (extracerebral) return to the detector closer to the original light source and thus can be separated from the interpretation of signals from the deeper target tissues (intracerebral) that take a longer path.78 The sample size of the brain tissue monitored, however, is small and represents only approximately 1 ml of brain.79

The cerebral oximeter provides a continuous measurement of the percentage of oxygenated hemoglobin residing in the tested intracerebral tissue. Because the ratio of arterial to venous blood is 15:85,80 the cerebral saturation measured primarily reflects cerebral venous saturation, ie, the balance between oxygen supply and demand. The only cerebral oximeter approved for use in the United States currently is the INVOS 4100 and 5100 (Somanetics Corp, Troy MI).

A major critique of the system is that there is no established normative range or threshold for pathologic change. In a study of healthy elderly noncardiac surgical patients, the mean baseline value was 63+/8%.81 However, a wide range of interpatient variability has been found.82 Other factors that can lead to variability include hemoglobin concentration of the measured site and pad positioning. A 20% decline from baseline values is the most commonly used indicator of pathologic change. It is based mostly on the findings of neurologic change after carotid artery occlusion during carotid endarterectomy.83,84 Another dilemma facing practitioners is what to do when faced with low starting baseline cerebral saturations and how to determine when pathologic changes occur in these patients. It has been estimated that 7% of patients have baseline saturations below 50%.82

The most validated use of cerebral oximetry in cardiac surgery is as a predictor of postoperative neurocognitive dysfunction and extended hospitalization in those patients who have prolonged cerebral desaturations in the operating room.85–87 Reports on the diagnosis and treatment of cerebral desaturation and presumed hypoperfusion during cardiac surgery include a diverse list of causes such as anemia, hypocapnia, extreme neck turning, SVC occlusion, and low perfusion pressure.79,88,89 There is also a growing list of reports of its utilization in guiding length of cooling and conduct of antegrade cerebral perfusion during aortic arch repair and circulatory arrest (Fig. 10-10).90–93 Although cerebral oximetry represents an exciting tool to monitor the adequacy of brain perfusion, issues with sensitivity and specificity remain, likely preventing a more widespread adoption currently. Embolic events to regions beyond the small sample sizes of brain will clearly be missed. To date there is only on randomized prospective study evaluating cerebral oximetry monitoring with a defined treatment algorithm.87

Motor and Somatosensory Evoked Potentials

The most common application of somatosensory evoked potential (SSEP) or motor evoked potential (MEP) monitoring in cardiothoracic surgery is for the detection of spinal cord ischemia during open or endovascular repair of the descending thoracic or thoracoabdominal aorta (Fig. 10-11).94–96 During these operations decreases in lower extremity SSEP or MEP amplitudes, indicating spinal cord ischemia, can be used to prompt interventions to increase arterial pressure, decrease lumbar CSF pressure, or reimplant segmental arterial branches in an effort to increase spinal cord perfusion to prevent paraplegia. The detection of reversible spinal cord ischemia by intraoperative MEP or SSEP monitoring may also identify patients who may be at risk for delayed postoperative paraplegia. Decreased SSEP and MEP amplitude have been shown to correlate with spinal cord ischemia, but the sensitivity and specificity of these techniques for detecting and reducing the incidence of spinal cord ischemia remains to be verified.97 Conditions other than spinal cord ischemia may produce MEP or SSEP changes.94

Intraoperative monitoring of SSEP is performed by placing stimulating electrodes on the skin adjacent to peripheral nerves in the arms or legs. Electrical stimulation of the peripheral nerves in the limbs generates action potentials that can be measured from recording electrodes over the lumbar plexus, brachial plexus, spine, brainstem, thalamus, and cerebral cortex. Motor evoked potentials (MEPs) are generated by transcortical electrical stimulation of the motor cortex that produces myogenic potentials that can be recorded in skeletal muscle. In theory, monitoring MEP should be more sensitive and specific than SSEP to detect spinal cord ischemia in the territory supplied by the anterior spinal artery. An advantage of SSEP monitoring is that it is relatively reliable and easy to interpret during general anesthesia without a contraindication to neuromuscular blockade. Although high concentrations of inhaled anesthetics, thiopental, or propofol can attenuate cortical SEP signals, a balanced general anesthetic with inhaled anesthetics maintained at a concentration of 0.5 MAC provide consistent conditions for monitoring intraoperative SSEP.

Detection of Cerebral Embolization

Intraoperative TEE, epiaortic ultrasound, and transcranial Doppler (TCD) are instruments that can be used to assess the risk and detect arterial embolic events (Fig. 10-12). The embolic burden to the cerebral circulation measured by quantitative TCD correlates with the incidence of intraoperative surgical manipulation and postoperative neurologic deficits.98 Intraoperative TEE can be applied to detect right-to-left intracardiac shunting through an atrial septal defect,99,100 intracardiac masses,101,102 or residual air within the cardiac chambers.103 Routine epiaortic ultrasonography or TEE to assess the degree of aortic atherosclerosis and guide the insertion of the aortic cannula and application of the aortic cross-clamp has been recommended for decreasing the risk of neurologic injury during CPB.104

Inhaled Anesthetics

Inhaled anesthetics alone produce all the conditions necessary for operation.105 The unit of concentration used clinically is termed minimum alveolar concentration, or MAC, which is defined as the concentration of volatile agent that produces immobility in 50% of people in response to a painful stimuli.106 The most commonly used inhaled anesthetics are isoflurane, sevoflurane, and desflurane. Isoflurane is older, less expensive, with a longer onset and recovery time. Desflurane has a short onset and a rapid recovery time but is pungent and can stimulate airway and sympathetic reflexes. Sevoflurane offers a lack of airway reactivity, a nonpungent odor, and minimal cardiovascular and respiratory side effects.107,108 The accumulation of compound A, a potential renal toxin and byproduct of sevoflurane use, has been associated only with low fresh gas flow (<1 L/min).

All inhaled anesthetics cause circulatory depression at concentrations necessary to produce general anesthesia. When ventilation is controlled, the circulatory actions of the inhaled anesthetics are what usually limit the anesthetic dose that can be tolerated, particularly in patients with cardiovascular disease. For this reason, lower doses of inhaled anesthetics usually are combined with other anesthetics, such as opioids, to produce a balanced general anesthetic for cardiac operations. The decrease in blood pressure caused by volatile anesthetics is a direct result of vasodilation and depression of myocardial contractility and an indirect result of attenuation of sympathetic nervous system activity. The decrease in blood pressure is so predictable that it is often used as a sign for assessing the depth of anesthesia. Overdose with inhaled anesthetics is manifested by hypotension, arrhythmias, and bradycardia that, if unrecognized, may lead to circulatory shock.

The inhaled anesthetics decrease myocardial contractility based on both experimental and clinical studies (Fig. 10-13).109–111 Inhalation anesthetics produce a dose-dependent decrease in mean maximal velocity of circumferential myocardial shortening, mean maximal developed force, and dP/dt.112–114 Isoflurane, desflurane, and sevoflurane decrease global left ventricular systolic function at any given left ventricular loading condition or at any given degree of underlying sympathetic tone (Fig. 10-14). Experimental studies suggest these agents cause minimal changes in left ventricular diastolic compliance but impair left ventricular diastolic relaxation in a dose-dependent manner.115 The effects of each individual inhaled anesthetic on cardiovascular function depend on selective dose-dependent effects of the drug on myocyte contraction and relaxation, vascular smooth muscle tone, and sympathetic nervous system reflexes; as well as the underlying disease state, intravascular volume status, surgical stimulation, temperature, mode of ventilation, and acid-base status. Despite a decrease in myocardial contractility, cardiac output generally is unchanged at 1.0 MAC of isoflurane because of direct arterial vasodilation and preservation of baroceptor reflexes, with a resulting decrease in ventricular afterload and increase in heart rate and stroke volume (Fig. 10-15).116

Although sympathetic nervous system activation owing to nociception may often mask clinical signs of circulatory depression caused by inhaled anesthetics, patients in shock or with profound ventricular dysfunction may not tolerate the cardiovascular depressant effects of inhaled anesthetics given in concentrations that are needed to produce anesthesia. Volatile anesthetics have a proportionally greater negative inotropic effect on diseased myocardium than on normal myocardium.

The administration of inhaled anesthetics in patients with preexisting cardiovascular diseases has potential advantages. The myocardial depressant and arterial vasodilatory actions of inhaled anesthetics decrease afterload and myocardial oxygen consumption, which benefits patients with coronary insufficiency creating a more favorable myocardial oxygen balance. In addition inhaled anesthetics are potent coronary vasodilators. Isoflurane causes endothelium-dependent inhibition of the contractile response of canine coronary arteries.117 However, anesthetic-induced hypotension may reduce coronary perfusion pressure and coronary blood flow.

Regional blood flow to other vital organs may be modified by inhaled anesthetics because of their effects on metabolic demands and autoregulation. The normal circulatory response to hypotension and low cardiac output is redistribution of blood flow to vital organs (ie, brain, heart, and kidneys) and a decrease in blood flow to skin, muscle, and the gastrointestinal system. Volatile inhalation anesthetics impair this protective response because of nonspecific vasodilation and can compromise vital organ perfusion if administered in high doses during periods of circulatory shock.

In general, carefully conducted clinical trials suggest that almost any inhaled anesthetic can be administered safely to patients with cardiovascular disease if the hemodynamic condition of the patient is optimally controlled.118

Sedative-Hypnotics

Sedative-hypnotics describe a broad class of anesthetic drugs that includes barbiturates, benzodiazepines, etomidate, propofol, and ketamine. They are used for preoperative sedation, can produce immediate loss of consciousness during intravenous induction of general anesthesia, supplement the actions of the inhaled anesthetics, and provide sedation in the immediate postoperative period. The circulatory effects of individual agents are an important consideration for patients with cardiovascular disease. The sedative-hypnotics can have direct effects on cardiac contractility and vascular tone, in addition to indirect effects on autonomic tone.

The barbiturates, such as thiopental or methohexital, are negative inotropic agents. They produce dose-dependent decreases in ventricular dP/dt and the force-velocity relationship of ventricular muscle.119 Induction of general anesthesia with a barbiturate is associated with a decrease in blood pressure and cardiac output. In comparison with barbiturates, propofol appears to cause less myocardial depression.120,121 The decrease in arterial pressure after propofol administration is attributed primarily to arterial and venous dilatation.122,123 Propofol is well suited for continuous intravenous infusion for sedation because it has a short duration of action and can be titrated to effect. Propofol given intravenously for sedation in a nonintubated patient requires the presence of an anesthesiologist because respiratory depression is common. Etomidate can be administered for rapid induction of general anesthesia in patients with preexisting hemodynamic compromise because it generally causes little or no change in circulatory parameters,124 except when patients are critically relying on elevated sympathetic tone. This agent is particularly useful for unstable patients undergoing emergency operation. Etomidate has virtually no effect on myocardial contractility even in diseased ventricular muscle.125,126 However, etomidate inhibits adrenal synthesis of cortisol by blocking beta-hydroxylase. This adrenal suppression effect has mostly been ignored when the drug is limited to short-term uses, such as an intravenous anesthetic induction. Newer data suggest this adrenal insufficiency may occur even following a single induction dose.127 The clinical relevance of this insufficiency remains to be determined.128

Ketamine often increases heart rate and blood pressure after anesthetic induction because it maintains sympathetic tone.129 The direct negative inotropic and vasodilating effects of ketamine can be unmasked when it is administered to critically ill patients with catecholamine depletion.130 Ketamine is not used routinely because it may cause postoperative delirium, especially if it is administered in the absence of other sedative-hypnotics.

Narcotic Anesthetics

Narcotics remain an important adjunct for cardiac anesthesia. Analgesic actions are mediated by direct activation of opioid receptors in the central nervous system, spinal cord, and periphery. Narcotic-based anesthetics offer the advantages of profound analgesia, attenuation of sympathetically-mediated cardiovascular reflexes in response to pain, and virtually no direct effects on myocardial contractility or vasomotor tone. Narcotics may be administered intravenously, intrathecally, or into the lumbar or thoracic epidural space. Even though narcotics have little direct action on the cardiovascular system, they may cause profound hemodynamic changes indirectly by attenuating sympathetic tone. Narcotics decrease serum catecholamine levels and produce cardiovascular depression indirectly, especially in a patient who are critically ill and dependent on endogenous catecholamines (eg, those with severe hypovolemia or cardiac tamponade). Morphine sulfate may decrease blood pressure by provoking the release of histamine.

Problems encountered with narcotic-based anesthetics include difficulty estimating the dose required because of patient variability, predicting the duration of postoperative narcotic-induced respiratory depression, and ensuring hypnosis during the operation. Rapid administration of narcotics is associated with muscle rigidity that may impede the ability to ventilate the patient immediately after the induction of general anesthesia.131 The rigidity usually affects the thoracic and abdominal musculature and is observed commonly with the larger doses of narcotic used in cardiac anesthesia. Myoclonic activity often associated with muscle rigidity easily can be mistaken for grand mal seizures. There is no evidence that opioids induce seizures when there is adequate oxygenation and ventilation.132 Opioid-induced muscle rigidity is readily reversed by the administration of neuromuscular blockers.

Opioid tolerance is represented by a decrease in response (both analgesia and respiratory depression) to a narcotic owing to prior exposure. Tachyphylaxis is the rapid development of drug tolerance without necessarily prior exposure. Drug dependence is a patient condition or disorder that occurs as a consequence of sustained exposure to a drug such that withdrawal or antagonism of the drug prohibits normal function.133 Perioperative exposure to morphine and synthetic narcotics is unlikely to produce the downregulation and desensitization of opioid receptors believed necessary for narcotic dependence.134 Cardiac surgical patients receiving narcotic infusions in the intensive-care unit often develop tachyphylaxis and require increasing doses to sustain the desired effect.135

Ultra–short-acting narcotics (eg, remifentanil) may have a unique niche in cardiac anesthesia because their effect is terminated almost immediately after discontinuing the drug infusion owing to rapid in vivo ester hydrolysis.136 Remifentanil successfully attenuates the sympathetic response to painful stimuli in cardiac surgery.137 Profound intraoperative analgesia can be provided while facilitating early resumption of respiration, consciousness, and extubation. Remifentanil can also be used to facilitate the use of motor evoked potentials to in order to monitor spinal motor pathways during thoracic aortic surgery.138

Neuromuscular Blocking Drugs

Neuromuscular blocking drugs are administered to facilitate intubation of the trachea, prevent patient movement during operation, improve surgical exposure of the operating field, and attenuate metabolic demands caused by potential shivering during hypothermia. Except for succinylcholine, the neuromuscular blocking drugs used in clinical practice are typically nondepolarizing competitive antagonists of acetylcholine at the nicotinic acetylcholine receptor of the motor end plate. Succinylcholine is an acetylcholine agonist that produces rapid, short-acting muscle paralysis by depolarizing the motor end plate.

Muscle relaxants are chosen based on the desired speed of onset, duration of action, route of elimination, spectrum of cardiovascular side effects, and cost (Table 10-4). The newer neuromuscular blocking drugs such as vecuronium and rocuronium have virtually no cardiovascular side effects and do not depend primarily on renal function for elimination. Cis-atracurium degrades spontaneously by pH- and temperature-dependent Hofmann elimination and is independent of both renal and liver function. Succinylcholine has the most rapid onset of action (90 seconds) but produces unpredictable changes in heart rate; increases serum potassium concentration by approximately 0.5 mEq/L; may cause life-threatening hyperkalemia in patients with denervation, burn, or compression injuries; and can trigger malignant hyperthermia in susceptible individuals. Pancuronium increases blood pressure and heart rate by blocking muscarinic acetylcholine receptors in the sinoatrial node, increases sympathetic activity via antimuscarinic actions, and inhibits reuptake of catecholamines.

Discontinuing general anesthesia or sedation before complete recovery from neuromuscular blockade is very distressing for patients because the awake, alert, and paralyzed patient has no means to communicate discomfort. Discontinuing mechanical ventilatory support in patients with residual neuromuscular blockade may cause acute or delayed respiratory failure. Even mild residual neuromuscular blockade contributes to pulmonary insufficiency by compromising mechanics of breathing and decreasing negative inspiratory force, vital capacity, tidal volume, and the ability to generate an effective cough. Muscle fatigue may produce airway obstruction by decreasing muscle tone in the oropharynx. Recovery from nondepolarizing neuromuscular blockade may be hastened by administering an acetylcholinesterase inhibitor such as neostigmine or edrophonium that decreases degradation of acetylcholine at the neuromuscular junction and thereby increases the concentration of the neurotransmitter at the motor end plate. The undesirable systemic effects of acetylcholine-esterase inhibitors are bronchospasm, bradycardia, and hypersalivation, which can be minimized by simultaneous administration of anticholinergic agents such as atropine or glycopyrrolate. Severe bradycardia has been described in heart transplant patients after reversal of neuromuscular blockade, possibly owing to the nonantagonized parasympathetic activity associated with acetylcholinesterase inhibitors in the denervated heart.139 Reliable reversal of neuromuscular blockade with cholinesterase inhibitors usually is achieved only after muscle strength has recovered spontaneously to approximately 25% of baseline levels. Recovery of neuromuscular function is usually measured by a transcutaneous nerve stimulator applied over the ulnar nerve just proximal to the hand with monitoring of thumb twitch strength.

Local Anesthetics

Local anesthetic drugs inhibit the propagation of action potentials in electrically excitable tissue by blocking sodium channels. Common local anesthetics used during anesthesia and surgery include lidocaine, bupivacaine, and ropivacaine. Lidocaine has a quick onset of action but a shorter duration of analgesia than the other two. Local anesthetics can be delivered by topical application to mucosa, infiltration into tissues, injection into the region of a peripheral nerve, infusion into the epidural space, or injection intrathecally into cerebrospinal fluid. Regional nerve blocks can be used to supplement a general anesthetic or to provide postoperative analgesia. Epinephrine often is added to local anesthetic solutions to prolong the anesthetic duration but may cause tachycardia or cardiac arrhythmias when absorbed into the systemic circulation.

Local anesthetic toxicity can occur because of systemic absorption of the injected drug or because of inadvertent direct intravascular injection. It can result in both neurologic and cardiovascular toxicity. The spectrum of neurologic symptoms extend from simply minor auditory and visual disturbances, progressing to motor twitching, and finally to grand mal seizures depending on the rise of local anesthetic blood levels. The blood concentration needed to produce neurologic symptoms can be low, particularly with a rapid injection, because of the high arterial supply of the brain. Most often neurologic symptoms are short lived as the drug is rapidly cleared, again because of high cerebral arterial flow. At higher drug blood levels, excitatory neurologic symptoms dissipate and central nervous system depression is seen, typically in conjunction with cardiovascular toxicity.

Cardiovascular toxicity is manifested by hypotension, cardiac arrhythmia, and myocardial depression, which may progress to complete cardiovascular collapse with electrical standstill. Bupivacaine has been noted to block cardiac sodium channels and thus conduction at blood levels just above that of seen with neurologic toxicity.140 Because of this, it is widely considered to have a higher degree of specific cardiac toxicity than ropivacaine. Bupivacaine has a slower disassociation from inactivated sodium channels then lidocaine, which likely contributes to its enhanced cardiotoxicity.140 Some authors, however, believe the increased cardiac toxicity to merely be related to a lower potency of ropivacaine versus bupivacaine and not to any intrinsic properties of bupivacaine.141 Treatment of local anesthetic toxicity includes traditional Advanced Cardiac Life Support (ACLS) including epinephrine but may necessitate brief cardiopulmonary bypass to allow for recovery. A novel therapy has recently been described with the use of lipid emulsion. Although the precise mechanism of action remains unknown, there have been numerous reports of miraculous recovery with its intravenous administration.142–144

Emergency Airway Management

Establishing a patent and secure airway is essential for the conduct of general anesthesia and is the first step in emergency life support for cardiovascular resuscitation. Tracheal intubation for airway protection and mechanical ventilation can be challenging in a patient with cardiovascular disease. General anesthesia is typically employed to facilitate tracheal intubation; however, the effects of general anesthetics produce respiratory depression and usually apnea in addition to vasodilation and cardiac depression. Difficultly with the establishment of an airway can create hypoxia and hypercarbia, and could potentially lead to cardiovascular collapse. The aspiration of gastric contents from an unprotected airway in an anesthetized or unarousable patient may also lead to pneumonitis. Inadequate anesthesia during tracheal intubation may provoke myocardial ischemia or tachyarrhythmias in susceptible patients. The American Society of Anesthesiologists has established practice guidelines for the emergency management of the difficult airway.145 The difficult airway (eg, Mallampati class 4) often can be intubated using fiberoptic bronchoscopy. This technique requires time and special equipment. The risk of hypertension, tachycardia, and discomfort during tracheal intubation in an awake patient can be offset partially by topical anesthesia and as well as light sedation. Fiberoptic intubation can also be achieved with the patient asleep, when mask ventilation is assumed to be acceptable, although the possibility that the establishment of an airway will be unsuccessful must be considered in this scenario.

Single-Lung Ventilation

Single-lung ventilation, or the ability to collapse one lung and selectively ventilate the contralateral lung, is necessary for operative exposure when the heart or great vessels are approached through a lateral thoracotomy incision. Selective lung ventilation is integral in the intraoperative management of patients undergoing minimally invasive direct coronary artery bypass (MIDCAB) procedures. Adequate surgical exposure with minithoracotomy for coronary revascularization without cardiopulmonary bypass requires deflation of the left lung. Single-lung ventilation is also used in patients undergoing thoracoscopic procedures, lung transplantation, open thoracic aortic operations, aortic or mitral valve surgery through a right thoracotomy, closure of large bronchopleural fistulas, intrathoracic robotic surgery, or life-threatening hemoptysis. Single-lung ventilation may be achieved using double-lumen endobronchial tubes (Fig. 10-16) or bronchial blockers (Fig. 10-17).

Wire-guided bronchial blocker kits often contain an adapter for use with a standard endotracheal tube and include ports for the bronchial blocker and fiberoptic bronchoscope. A central lumen for the blocker contains a monofilament loop that passes out the end of the catheter. Placement of the loop over a fiberoptic bronchoscope permits the bronchial blocker to be guided directly into position using the bronchoscope. Removal of the monofilament loop from the central lumen provides a port for venting the nonventilated lung. Other styled blockers have a steerable tip that can be visualized through the bronchoscope and manipulated into a main bronchi. Bronchial blockers for lung isolation are preferred when the larynx is too small to accommodate a double-lumen endobronchial tube or in a patient with an anticipated difficult airway. This is because the larger double-lumen endobronchial tube is often more challenging to place than a smaller single lumen tube. Also, because of the design of the double lumen tube, adjunctive intubation strategies are more difficult than with a single lumen tube. A bronchial blocker may also be chosen when it is difficult or dangerous to change an in situ endotracheal single lumen tube, or when the trachea or main stem bronchus are distorted by a mediastinal mass or aortic aneurysm. The routine use of fiberoptic bronchoscopy has decreased the complication rate and uncertainty regarding positioning of these devices in the airway.

Controlling Lumbar Cerebrospinal Fluid Pressure

Spinal fluid drainage may improve neurologic outcome from spinal cord ischemia during thoracic and thoracoabdominal aortic operations.146–148 Based on evidence from meta-analysis of randomized and nonrandomized clinical trials, lumbar CSF drainage is recommended as part of a multimodal approach to prevent paraplegia after thoracoabdominal aortic surgery.149,150 The physiologic rational of lumbar CSF drainage is to improve spinal cord perfusion pressure, which is approximated by the difference between the mean arterial pressure and the CSF pressure.151 Based on this principle, successful application of CSF drainage also requires interventions to increase arterial pressure and to decrease the central venous pressure.151,152 CSF drainage is achieved by aseptic insertion of a subarachnoid catheter through a Tuohy needle positioned in a lower lumbar vertebral interspace. The insertion of a CSF drain before anticoagulation for extracorporeal circulation appears safe.151,153 The catheter typically is inserted the night before an operation or 1 to 2 hours before systemic anticoagulation. CSF is drained passively to reduce lumbar CSF pressure to approximately 10 to 12 mm Hg during operation. CSF drainage is continued typically for 24 to 48 hours after an operation. In the absence of spinal cord ischemia, the catheter is capped for another 24 hours before removal. Emergent implementation of lumbar CSF drainage to a target lumbar CSF pressure of 10 mm Hg, combined with augmentation of the mean arterial pressure to 100 mm Hg, has been reported to be effective for the treatment of delayed-onset paraplegia or paraparesis after thoracic and thoracoabdominal aortic reconstruction.151 Complications associated with lumbar CSF catheters include meningitis, persistent CSF leak, breakage and retention of catheter fragments, and hemorrhage.154–156 Intracranial hypotension is an important complication of lumbar CSF drainage and is believed to contribute to the risk of subdural hematoma.157 The risk of intracranial hypotension can be managed by continuously monitoring CSF pressure and the volume of CSF drained. The risk of hemorrhagic complications can be managed by ensuring adequate platelet and coagulation function during both the insertion and removal of the lumbar CSF drain.

Regional Anesthesia and Analgesia

Epidural or intrathecal (neuraxial) administration of local anesthetics and narcotics can provide profound postoperative analgesia after cardiac surgical operations with less sedation or respiratory depression than parenteral narcotic analgesia.158–160 A continuous infusion or intermittent bolus technique can be used. Patient-controlled epidural analgesia (PCEA) can also be triggered by patient demand with a predetermined maximum lockout to help prevent overdose. PCEA is an effective method to titrate the dose of epidural local anesthetic and/or narcotic based on clinical need. The potential clinical advantages of epidural or intrathecal analgesia are less postoperative pain, decreased duration of postoperative ventilatory support, attenuation of the surgical stress responses, and improved pulmonary function.161

The most common side effect of neuraxial analgesia is hypotension caused by local anesthetic blockade of the preganglionic vasomotor efferents of the sympathetic nervous system and loss of compensatory vasoconstriction. The potency of this side effect can be lessened by decreasing the concentration of the local anesthetic used. Respiratory depression can occur with systemic absorption of epidural narcotics or the rostral rise in the CSF with intrathecal administration. The onset of respiratory depression can be unpredictable and can sometimes be quite delayed. Nausea and pruritus are also common side effects of epidural or intrathecal narcotics. Epidural hematoma formation leading to spinal cord compression is a rare but potentially catastrophic complication of epidural and intrathecal analgesia, with an estimated frequency of 1 in 150,000 patients.162 Instrumentation of the epidural space during the performance of neuraxial anesthesia or the removal of a catheter is contraindicated in anticoagulated or coagulopathic patients.163,164

Epidural or intrathecal catheters are most often inserted before the operation, typically before the induction of anesthesia. This theoretically allows the conscious, but usually sedated patient, to report pain associated with needle and/or catheter-induced paresthesias or with drug administration, which could represent intraneural injection. Pain during needle placement or with the injection of local anesthetic has been associated with neurologic injury during regional anesthesia.165,166 The performance of neuraxial anesthesia before induction allows for maximizing the time between needle placement and systemic heparinization, which must be at least 1 hour. In some centers, epidural or intrathecal catheters are placed the night before surgery when full dose anticoagulation is employed for cardiopulmonary bypass to increase the safety margin.

As alluded to above, concern for epidural hematoma leading to spinal cord compression and possibly permanent paralysis during or after cardiopulmonary bypass in patients who receive full systemic heparinization remains paramount. The American Society of Regional Anesthesia, in their 2002 consensus statement, determined that although neuraxial anesthesia in patients who subsequently receive low-dose heparin in vascular surgery has proved to be safe, the safety in patients receiving full systemic heparinization for cardiac surgery requires further study.167 There are an increasing number of recent reports describing the successful use of both spinal and epidural anesthesia for cardiac surgery.168–170 This evidence, in addition to data from the successful use of CSF catheters in cardiac surgery, would suggest that the incidence of epidural hematoma formation in carefully selected patients is low. However, currently, there still is insufficient evidence to properly characterize the risks and especially the benefits of neuraxial anesthesia compared with more conventional anesthetic techniques and this has continued to preclude the widespread acceptance of neuraxial anesthesia in cardiac surgery.171

Minimal Invasive Cardiac Surgery

The widespread adoption and expansion of minimally invasive cardiac surgery has presented the cardiac anesthesiologist with many new challenges. Because of a limited exposure to the heart and great vessels, the cardiac surgeon relies heavily on the cardiac anesthesiologist to assist in these cases. It is common for the anesthesiologist to be requested to pericutaneously place cannulas that are traditional placed directly in the surgical field. Examples include large venous drainage cannula (14 to 21 French) placed in the right internal jugular vein (IJV) to provide venous inflow to the bypass circuit, retrograde cardioplegia cannula (EndoPlege Sinus Catheter, Edwards Lifesciences LLC, Cardiovations) advanced into the coronary sinus from the right IJV (Fig. 10-18), a pulmonary artery vent to decompress the left heart during bypass, and pacing wires advanced through a specialized pulmonary artery catheter. Lung isolation is also typically requested during surgery involving a thoracotomy incision. In addition to performing new specialized procedures, minimally invasive cardiac surgery also requires intensive TEE examinations. Not only is it important because of the limited ability for direct surgical inspection of the heart and great vessels, TEE is critical for the placement and/or confirmation of most of the surgical cannulas used during minimally invasive cardiac surgery. The use of an endoaortic balloon (EndoClamp Aortic Catheter, Edwards Lifesciences LLC, Cardiovations) also mandates TEE guidance for proper positioning in the ascending aorta (Fig. 10-19).

Cardiac surgery is conducted in an interdisciplinary environment among surgeon, anesthesiologist, perfusionist, and nursing staff. Since the release of the Institute of Medicine report To Err is Human in 1999, there has been an increased awareness of the impact of medical errors on health care.172 The use of crew resource management has been identified as an important component to reduce medical errors in the surgical arena.173 The cardiac anesthesiologist is in a unique position to take on a leadership role in such patient safety activities, including pre- and postoperative briefing-debriefing sessions and patient safety “time outs.”

The anesthetic begins before the patient arrives in the operating room. The patient's identification and scheduled procedure are verified immediately before and again after arrival in the operating room. The physical condition of the patient is assessed clinically, and medical events that occurred over the previous 12 to 24 hours are reviewed. For elective surgery, the patient should have fasted for a minimum of 8 hours before induction of general anesthesia, although it has become debatable whether 8 hours is necessary. Patients are often premedicated with a sedative-hypnotic (eg, a benzodiazepine) and/or an analgesic (eg, fentanyl) unless the associated mild degree of respiratory depression would be considered dangerous.

The patient is escorted into the operating room and placed onto the operating table. The operating room requires a minimum of 800 ft2 to comfortably accommodate the patient, health-care providers, standard operating room equipment, intraoperative cell salvage machine, heart-lung machine, and assist devices, if needed.174 The required square footage may be greater for the higher-technology procedures such as robotic surgery. Routine noninvasive monitors are applied and prophylactic antibiotics are administered with the goal of antibiotic completion in adequate time before incision. An arterial catheter is inserted, most often in the radial artery. A blood sample is acquired for laboratory analysis, and a blood type and crossmatch are requested, if not done already. A central venous catheter is always indicated, although in many patients it can be inserted after the induction of general anesthesia. A pulmonary artery catheter is used commonly to provide measures of cardiac output and estimates of ventricular filling pressures.175 Large-bore intravenous catheters are often inserted for patients, particularly in those who are undergoing reoperation because of the possibility of rapid blood loss during sternotomy. The immediate availability of typed and cross-matched blood is verified before skin incision. External defibrillation pads are applied to patients undergoing reoperation or in procedures in which access to the heart with internal paddles would not be readily available.

Induction of general anesthesia is achieved by intravenous administration of sedative-hypnotics, inhalation of volatile potent anesthetics, or both, most often in conjunction with opioids. Inhalation inductions permit maintenance of spontaneous ventilation and a controlled titration of anesthetic dose but prolong the excitatory phase of anesthesia when the patient is prone to cough, move, develop laryngospasm, or vomit and aspirate. Inhalation inductions are not commonly used in adults. Intravenous induction produces rapid apnea that requires immediate ventilatory support. Administration of neuromuscular-blocking drugs produces profound muscle paralysis and facilitates laryngoscopy and tracheal intubation. Vasoactive drugs are titrated, if necessary, to counteract the cardiovascular effects of anesthetics and loss of sympathetic tone. Laryngoscopy is extremely stimulating and, if the patient is inadequately anesthetized, may cause hypertension, tachycardia, or stimulate vasovagal reflexes. Most adult patients can be intubated with an 8.0-mm internal-diameter polyvinyl chloride endotracheal tube that accommodates an adult flexible bronchoscope. The tip of the tracheal tube is secured above the carina by documenting breath sounds bilaterally.

The patient is positioned before surgical preparation and draping, typically with the arms tucked at the side and a shoulder roll under the scapula. Regions susceptible to pressure injuries are protected and padded, and the patient is positioned to decrease pressure on the postcondylar groove of the humerus.176 ECG wires, tubes, and lines are not run under the arm. The incorporation of a simple examination of extremity nerve function during the postoperative visit provides a means to detect peripheral nerve injury.

Maintenance of general anesthesia is achieved by continuous or intermittent administration of anesthetic drugs titrated to effect while monitoring the conduct of the operation and vital physiologic functions. Anesthetics are chosen based on the patient's preoperative cardiovascular function, drug pharmacokinetics, and the dose-dependent pharmacologic actions. Surgical incision in the presence of inadequate concentrations of a volatile or intravenous anesthetic produces hypertension, tachycardia, tachypnea, and movement. In the absence of stimulation, the same anesthetic produces cardiovascular depression, hypotension, and apnea. The anesthesiologist titrates the anesthetic to a measurable end point by monitoring effects. As anesthetics are increasingly tailored for rapid emergence, lower doses and shorter acting medications are often employed that may predispose to intraoperative awareness if patient response is not closely monitored. Decisions to administer benzodiazepines prophylactically may be prudent in selected patients, such as those with a history of drug resistance or tolerance and young age. High doses of benzodiazepines may preclude early emergence.

Short-acting vasoactive agents with rapid onset of action usually are preferred for controlling hemodynamics because conditions can change rapidly. Vasopressors and inotropic agents sometimes are required to support the circulation in response to anesthetic-induced vasodilation and cardiac depression. Using nitroglycerin to modify venous capacitance permits buffering acute changes in intravascular volume. Heart rate can be controlled by short-acting cardioselective beta-adrenergic agonists and antagonists, vagolytic agents, or chronotropic drugs or, alternatively, by direct cardiac pacing. The urgency to control hemodynamic parameters with pharmacologic therapy must be tempered by recognizing the risk of drug overdose from overzealous treatment. Intraoperative events associated with acute increases in anesthetic requirements are sternotomy, chest wall retraction, manipulation and cannulation of the aorta, rewarming during cardiopulmonary bypass, and sternal wiring. Intraoperative awareness from insufficient anesthesia may occur during cardiac surgery, especially if a greater emphasis is placed on avoiding cardiovascular actions of anesthetic agents than on providing sufficient anesthesia.

Initiation of cardiopulmonary bypass acutely changes circulating drug concentrations. The addition of 2 L of pump prime has a negligible effect on plasma concentrations of lipophilic drugs with a large volume of distribution but significantly decreases the concentration of drugs distributed primarily in the intravascular space. Despite measurable decreases in blood anesthetic concentrations during cardiopulmonary bypass, the anesthetic level may not change because systemic hypothermia decreases anesthetic requirements, potentiates the effects of neuromuscular blocking drugs, and increases the solubility of volatile anesthetics in blood. Rewarming returns anesthetic requirements to baseline levels and predisposes to inadequate anesthesia if therapeutic drug concentrations are not maintained. The judicious use of sedative-hypnotics, analgesics, and amnestic agents during rewarming decreases the incidence of recall but does not guarantee unconsciousness. Volatile inhalation anesthetics can be given during cardiopulmonary bypass by adding them to the oxygen-rich gas mixture ventilating the pump oxygenator. This use of volatile anesthetics requires an effective scavenging system to prevent accumulation of anesthetic gases in ambient air.

Separation from cardiopulmonary bypass requires effective communication among members of the intraoperative team. Similar to an airline pilot preparing to land, the cardiac anesthesiologist has a checklist that ensures that all systems are in working order (Table 10-5).

The importance of a check list cannot be overstated, because many tasks must be incorporated into a successful separation from cardiopulmonary bypass and in the difficult cases it may be easy for a distraction to lead one to forget a critically important component. Beyond ensuring adequate anesthesia, careful management of the patient's hemodynamics is necessary. Anesthetic induced changes in vascular tone and cardiac function are now often superimposed on post cardiopulmonary bypass systemic inflammation and myocardial stunning. A TEE examination is usually performed to assess the adequacy of cardiac filling, contractility, and valvular function, as well as confirming a successful surgical result. Occasionally, findings from the TEE exam will necessitate a return to cardiopulmonary bypass and further surgical intervention. An arterial blood sample is obtained following protamine administration to ensure adequate heparin reversal and for arterial blood gas analysis. Continued bleeding after heparin neutralization indicates the need for further surgical hemostasis or the administration of the platelet concentrates, coagulation factors, or anti-fibrinolytics. After the sternum is reapproximated and the wounds closed and dressed, the patient is prepared for transport. Before departing the operating suite for the intensive care unit (ICU), pertinent patient information should be communicated to the critical care unit team about to accept the patient in order to facilitate transfer of care on arrival.

Continuous visual inspection of the patient and continuous monitoring of pulse oximetry, blood pressure, and ECG during transport to the postoperative ICU is standard. Meticulous attention is necessary from all members of the operating team even though the operation is completed, because the transition from operating room to ICU is fraught with risk. Transport usually entails a decrease in monitoring compared to the controlled setting of a cardiac OR. Smaller, sometimes less reliable, transport monitors replace the large screens with multichannel leads and pressure waveforms. Capnography is not typically monitored during transport. Occult bleeding into the chest with the chest tubes off suction may manifest itself during transport and early signs may be nonspecific and limited to hypotension, respiratory variations in the blood pressure tracing, or passive drainage of blood into the chest tubes. The discontinuation of anesthetic gases without supplementation with intravenous agents may result in an early, unanticipated emergence from general anesthesia. Intravenous sedative-hypnotic or analgesic drugs administered in the immediate postoperative period to treat surgical manipulation may contribute to hypotension during transport as stimulation has decreased. Conversion from the anesthesia machine ventilator to a hand-bag assembly for controlled ventilation (eg, Mapleson system) often results in hypoventilation. Careful attention must also remain on the patient's intrinsic rhythm and temporary pacemaker function.

Anesthesia is often extended into the early postoperative period because of the need for mechanical ventilatory support, treatment of hypothermia, and management of pain. Hypertension and tachycardia occur in the setting of tracheal intubation if abrupt emergence occurs. Several hours may be needed to achieve criteria required for tracheal extubation (eg, minimal bleeding, cardiovascular stability, and systemic rewarming). Vasodilation and increased cutaneous blood flow with active rewarming typically occurs after arrival into the intensive care unit. Postoperative positive-pressure ventilation is often quite different with the chest closed. Tidal volumes may be decreased, especially in the setting of an in situ internal mammary graft, because the expanding lung can impinge on the pedicle graft and place tension on the fresh suture lines. Arrival in the intensive-care unit triggers a battery of laboratory tests designed to assess rapid changes in vital organ function and prompt corrective therapy. These tests include a chest radiograph, ECG, complete blood and platelet count, chemistry battery with blood urea nitrogen and serum creatinine determinations, a serum glucose determination, prothrombin time and partial thromboplastin time, and arterial blood gas determination.

Preemptive patient management during the operation and in the early postoperative period can decrease intensive-care-unit and hospital length of stay after cardiac surgery.177 Traditionally, high-dose narcotic anesthesia provided profound analgesia, sympathetic blockade, and a gradual emergence that was managed over a time course of 8 to 12 hours. With high-dose narcotic anesthesia, patient recovery often was determined by the duration of action of the anesthetic given in the operating room. The time required for recovery from general anesthesia may be decreased by short-acting sedative-hypnotics (eg, propofol) or analgesics administered by infusion that continues into the postoperative period and permits recovery according to the patient's condition rather than the anesthetic. Implementation of protocol-based care plans designed to expedite patient recovery after cardiac operations requires a coordinated effort and mutual understanding between the anesthesiologist, surgeon, and critical care team.