Advanced Search

Savino JS, Floyd TF, Cheung AT. Cardiac Anesthesia.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:249281.

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this book
Right arrow Author home page(s):
Albert T. Cheung
Google Scholar
Right arrow Articles by Savino, J. S.
Right arrow Articles by Cheung, A. T.
Right arrow Articles citing this Article
Right arrow Search for Related Content
PubMed
Right arrow Articles by Savino, J. S.
Right arrow Articles by Cheung, A. T.
Related Collections
Right arrow Anesthesia

Chapter 9

Cardiac Anesthesia

Joseph S. Savino/ Thomas F. Floyd/ Albert T. Cheung

PREOPERATIVE EVALUATION
MONITORING PHYSIOLOGICAL FUNCTIONS DURING ANESTHESIA
????Measurement of Blood Pressure
????Electrocardiogram
????Capnography
????Pulse Oximetry
????Measurement of Temperature
????Measurement of Cardiac Output and Central Venous and Pulmonary Artery Pressures
????Anesthetic Gas Monitors
????Measurement of Electrolyte Concentration
????Monitoring the Nervous System
????????STROKE
????????PARALYSIS
????????COGNITIVE DYSFUNCTION
????????NEUROLOGIC SEQUELAE IN NONCARDIAC SURGERY
ANESTHESIA
????Anesthetics and Neuromuscular Blockers
????????INHALED ANESTHETICS
????????SEDATIVE-HYPNOTICS
????????NARCOTIC ANESTHETICS
????????NEUROMUSCULAR BLOCKING DRUGS
????????LOCAL ANESTHETICS
????Special Anesthetic Techniques
????????EMERGENCY AIRWAY MANAGEMENT
????????SINGLE-LUNG VENTILATION
????????REGIONAL ANESTHESIA AND ANALGESIA
????????CONTROLLING LUMBAR CEREBROSPINAL FLUID PRESSURE
THE CONDUCT OF ANESTHESIA, SURGERY, NURSING, AND PERFUSION
ANESTHESIA IN THE IMMEDIATE POSTOPERATIVE PERIOD
REFERENCES

?? INTRODUCTION
 Top
 Next
 References
?
The objectives of a general anesthetic are to provide the patient with analgesia, amnesia, and unconsciousness while supporting vital physiologic function and creating satisfactory operating conditions. An effective general anesthetic prevents patient movement and blunts the physiologic responses to surgical trauma, nociception, and hemodynamic perturbations and permits recovery at a predictable time after 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 during surgical incision, rapid changes in body temperature, extracorporeal circulation, and acute shifts in intravascular volume. 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. Furthermore, anesthetic management of the cardiac surgical patient is intimately related to the planned operative procedure and the anticipated timing of intraoperative events.

The choice of general anesthetics is often dictated by the patient's preoperative cardiovascular function, drug pharmacokinetics, and the dose-dependent pharmacologic actions of the anesthetics. Surgical incision in the presence of inadequate concentrations of a volatile 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 cardiovascular effects. There is no direct method for assessing or monitoring adequacy of analgesia or state of awareness in a paralyzed patient, although the BIS monitor offers some insight. The BIS monitor is an integrated EEG system that relates a bispectral index to depth of general anesthesia.1,2


?? PREOPERATIVE EVALUATION
 Top
 Previous
 Next
 References
?
The preoperative visit by the anesthesiologist is aimed at formulation of an anesthetic plan based on the patient's surgical illness, scheduled operation, and concomitant medical problems. The anesthesiologist is responsible for informing the patient of the conduct of the planned anesthetic and associated risks and obtaining consent for the anesthesia and related procedures. The medical history is elicited by questioning the patient and reviewing the medical records. The nature and severity of the surgical illness and related cardiovascular and pulmonary disease often dictate the choice of anesthetic drugs and monitors. All anesthetic drugs have a direct effect on cardiac function, vascular tone, or the autonomic nervous system. The anesthesiologist must know the status of the cardiovascular system, related morbidity, and concurrent medications to safely design the anesthetic for a patient undergoing heart surgery.

The exchange of information between patient and physician is often a balance between providing sufficient insight regarding possible complications and producing harmful anxiety. An outline of upcoming events accompanied by an informative discussion of risks and options usually leads to informed consent. Laboratory tests are ordered to complement findings of the medical history and physical examination. Routine preoperative tests for patients scheduled for a cardiac operation include a complete blood and platelet count, electrolyte battery, determination of blood glucose, serum creatinine, and blood urea nitrogen levels, prothrombin time and partial thromboplastin time, chest radiograph, electrocardiogram (ECG), and urinalysis.

The American Society of Anesthesiologists (ASA) has developed a physical status classification as a general measure of the patient's severity of illness (Table 9-1).3 Concurrent medical illness often defines an acceptable range for monitored parameters that are controlled during cardiac surgery, contributes to postoperative morbidity, or influences the response to a specific drug. Acceptable intraoperative blood pressure is defined by the range of blood pressure before surgery. A severely hypertensive patient may inadequately perfuse vital organs if the blood pressure during surgery is maintained within a "normal" range rather than within the patient's usual range. A previous stroke with apparent recovery may become manifest after general anesthesia without evidence of a new neurologic injury. Chronic obstructive pulmonary disease and its response to bronchodilators permit guided management of perioperative bronchospasm and inadequate respiration. Prior surgical and anesthetic procedures are investigated by reviewing medical records. A history of a difficult intubation or adverse response to a specific drug is highly relevant to the anesthesia plan.


View this table:
[in this window]
[in a new window]
?
TABLE 9-1 American Society of Anesthesiologists' physical status classification

?
Concurrent medications usually are continued until the operation, although the dose may be altered or a shorter-acting preparation substituted. Oral medications are administered according to schedule on the day of surgery with a small sip of water. Intravenous heparin given for unstable angina pectoris is not discontinued before surgical incision. For patients scheduled for late afternoon surgery and not receiving maintenance intravenous fluids, preoperative diuretics may be withheld to avoid dehydration. The physical examination includes measurement of vital signs and height and weight and a comprehensive assessment of the heart, lungs, peripheral vasculature, nervous system, and airway. Samsoon's modification of the Mallampati classification to predict a difficult airway is based on the examiner's ability to view intraoral structures4,5:
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 operation frequently is incompatible with leisurely preparation but is dictated by a sense of urgency. Rarely is there no opportunity to provide reassurance or to meticulously prepare for anesthesia and operation.


?? MONITORING PHYSIOLOGICAL FUNCTIONS DURING ANESTHESIA
 Top
 Previous
 Next
 References
?
Extensive physiological monitoring is employed during cardiac operations because virtually every major physiological system required for life is affected. The reasons for physiological monitoring are: (1) to ensure patient safety in the absence of protective reflexes made ineffective by anesthetic drugs; (2) to enable pharmacological 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 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. In setting up a monitoring and diagnostic system, it is important to establish the sensitivity and specificity for detecting physiological changes and disease. Sensitivity is a measure of the ability of a monitor to detect change in whatever is measured (measurand). Specificity is the degree that a change in the measurand is peculiar to a singular condition or disease. Sensitivity and specificity of a monitor depend on sensor calibration, accuracy, and precision. A sensor is an instrument that detects change in the measurand and provides a corresponding output signal. Calibration is the relationship between the measurand and the output signal, such that the magnitude of the output signal reflects the magnitude of the parameter being measured. Pressure transducers, light detectors, flowmeters, thermistors, and gas analyzers are examples of sensors commonly used in the operating room. The ideal sensor is accurate during static and dynamic conditions, precise, reliable, safe, practical, and inexpensive. Accuracy is defined by how well the output signal agrees with the true value or a calibration quality standard. Precision is a measure of repeatability. A sensor is precise if it provides little variability between repeated measures. A pulse oximeter is an accurate monitor of percentage of oxyhemoglobin because it agrees with in vitro measures (between values of 80% to 100%). Thermodilution is an imprecise method of determining cardiac output because successive measurements vary by 20% or more. All monitors are properly calibrated prior to clinical use, and specifications for accuracy and precision must be established to maximize sensitivity and specificity for detecting diagnosing change.

The selection of monitors is dictated by the utility of the generated data, 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 (e.g., esophageal stethoscope during esophageal surgery) (Table 9-2). Other noninvasive and invasive monitors are used only with clear indication.


View this table:
[in this window]
[in a new window]
?
TABLE 9-2 Physiological monitors

?
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 do not influence medical or surgical management. Improved safety decreases patient morbidity and mortality, decreases the direct costs of health care providers, and reduces legal costs, insurance premiums, and possibly the risk of early retirement by physicians. However, monitors do not interpret data and must themselves be monitored by a human being.

Measurement of Blood Pressure

Blood pressure changes abruptly during anesthesia and surgery and is the most commonly measured index of cardiovascular stability in the perioperative period. Anesthetics and surgery cause changes in blood pressure that may be great enough to cause harm unless anticipated and treated. A change in blood pressure alters perfusion pressure but may not change organ blood flow. Most vital organs have autoregulation of blood flow in response to changes in mean arterial blood pressure, permitting a constant blood flow over a range of perfusion pressures.6 In hypertensive patients, the boundaries for autoregulation are shifted so that significant decreases in organ perfusion may occur with blood pressures in the "normal" range. Both the type and dose of anesthetic medications affect the relationship between vital organ perfusion and blood pressure. Volatile anesthetics are potent vasodilators that tend to disrupt autoregulation in a dose-dependent manner to render blood flow more linearly dependent on blood pressure (Fig. 9-1).



View larger version (22K):
[in this window]
[in a new window]
?
FIGURE 9-1 Autoregulation maintains a constant cerebral blood flow between mean arterial blood pressures of 50 to 150 mm Hg in the conscious, unanesthetized state. Increasing doses of potent inhalation anesthetics produce a dose-dependent disruption of autoregulation due to cerebral vasodilatation. (Modified with permission from Shapiro H: Anesthesia effects upon cerebral blood flow, cerebral metabolism, electroencephalogram and evoked potentials, in Miller RD (ed): Anesthesia, 2d ed. New York, Churchill-Livingstone, 1986; p 1249.)

?
Although noninvasive blood pressure monitoring suffices for most patients during routine noncardiac surgery, direct measure of arterial blood pressure with an indwelling catheter is necessary for cardiac surgery in order to detect changes rapidly, to measure nonpulsatile blood pressure during cardiopulmonary bypass, and to facilitate 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 is typically 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 intra-arterial cannula, tubing, and transducer assembly are prepared prior to surgery and flushed with heparinized saline. All air bubbles must be cleared from the system to prevent damping and air embolism. The radial artery is the most common site for the insertion of an intra-arterial catheter. The increased use of arterial conduits for coronary grafts limits the possible sites for monitoring. Twenty-gauge catheters are preferred because larger catheters are more likely to cause thrombosis. Thrombosis of the radial artery does not produce ischemia of the hand and fingers in the presence of intact ulnar blood flow and a patent palmar arch although distal emboli remain a risk. The Allen 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.7 Other sites selected for the insertion of an intra-arterial catheter 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.8 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.9,10 The blood pressure waveform measured in the ascending aorta is minimally affected by reflected waves in contrast to the measurement of blood pressure in the dorsalis pedis or radial artery. Vasodilators decrease terminal impedance at the artery-arteriolar junction and decrease the resonant frequency of the arterial waveform.

The contour of the pressure waveform is 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 (extension tubing, catheter, stopcocks) is close to the frequency of the pressure waveform.8 The natural or resonant frequency fn of a monitoring system is defined by

where C = compliance of the measuring system, L = length of the tubing, D = diameter of the catheter extension tubing, and p = 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.11 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.12 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 faithfully reproduced. A simple test is the brief flush of a high-pressure heparinized 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 suggest overdamping. A rapid return to baseline followed by sustained oscillations suggests ringing.

Electrocardiogram

The intraoperative electrocardiogram (ECG) monitor has evolved from the fading ball oscilloscope to a sophisticated microprocessor analog display. ECG signals are digitally filtered 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. 9-2). Together, these leads detect greater than 90% of ischemic episodes in patients with coronary artery disease who have noncardiac surgery.13 The ECG leads selected for monitoring of myocardial ischemia can be guided by preoperative testing. Myocardium at risk, identified by exercise testing or coronary angiograms, can be monitored by selecting the lead with the appropriate vector. A reversible perfusion defect of the inferior wall of the left ventricle during an exercise thallium reperfusion scan may encourage the anesthesiologist to specifically monitor leads II, III, and AVF.



View larger version (29K):
[in this window]
[in a new window]
?
FIGURE 9-2 Standard intraoperative electrocardiogram (ECG) lead placement. Typically, leads II and V5 are continuously monitored.

?
Diagnostic criteria for myocardial ischemia based on the ECG are (1) acute ST-segment depression greater than 0.1 mV 60 msec beyond the J point or (2) acute ST-segment elevation greater than 0.2 mV 60 msec beyond the J point (see Fig. 9-3).14 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.



View larger version (27K):
[in this window]
[in a new window]
?
FIGURE 9-3 Automated ST-segment monitoring of the ECG can be used to detect intraoperative myocardial ischemia. General criteria for myocardial ischemia are ST-segment depression greater than 0.1 mV or ST-segment elevation greater than 0.4 mV that persists for longer than 1 minute. At fast heart rates, the ST-segment measurement point may occur on the upslope of the T wave, causing erroneous indication of ST-segment elevation.

?
Digital signal processing handles much larger quantities of information compared to 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 (see Fig. 9-3). Because the accuracy of automated ST-segment monitoring is vulnerable to baseline drift and dependent on the 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 the 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 only be measured 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 toxic drug effect (quinidine or procainamide). The electrically dormant heart during aortic cross-clamping and perfusion with cold cardioplegia is monitored by the ECG. Hypothermia decreases action potential conduction velocity and high-dose potassium decreases the transcell 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. 9-4). Changes in its contour reflect disorders of ventilation, carbon dioxide production, or carbon dioxide transport to the lungs. 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. A steep increase in the phase 3 slope in the exhaled CO2 concentration suggests partial airway obstruction, either mechanical (tube kinking) or physiologic (bronchospasm). A progressive decrease in exhaled carbon dioxide concentration occurs with decreased CO2 production (hypothermia), increased minute ventilation, increase in physiologic dead space ventilation (e.g., pulmonary embolus), or low cardiac output. A progressive increase in exhaled carbon dioxide concentration occurs with hypoventilation, increased CO2 production (malignant hyperthermia), or increased delivery of CO2 to the lungs, such as occurs during weaning off bypass. The contour of the capnogram is also affected by the expiratory flow rate, distribution of pulmonary blood flow, distribution of ventilation, and the use of sidestream or mainstream carbon dioxide analyzers. Despite the interplay of mechanical and physiologic factors that affect the shape of the capnogram, any abrupt change in contour always signifies an acute change in the patient's cardiovascular, pulmonary, or metabolic state.



View larger version (8K):
[in this window]
[in a new window]
?
FIGURE 9-4 The normal capnogram: (1) inspired CO2 concentration = zero, (2) washout of anatomic dead space, (3) plateau represents alveolar gas CO2 content, and (4) beginning of inhalation.

?
Pulse Oximetry

Pulse oximeters were universally adopted into the practice of anesthesia almost immediately after their introduction despite lack of data demonstrating improved outcome with their use. Oxyhemoglobin saturation and arterial oxygen tension are measured routinely during cardiac surgery by intermittent arterial blood sampling. Arterial blood gas analysis does not replace the pulse oximeter, which continuously measures arterial hemoglobin saturation and pulse rate. The pulse oximeter detects decreasing percentages of oxyhemoglobin before changes in the color of the patient's skin or blood are evident.15 The pulse oximeter is reusable, inexpensive, and noninvasive, and provides continuous online data. Its major limitations include electrical interference, motion artifact, high failure rate during periods of low flow or inadequate perfusion, and the need for pulsatile flow for proper operation.16

Pulse oximetry measures the percentage of oxyhemoglobin in arterial blood by transillumination and detection of differences in the optical absorption properties of oxy- and deoxyhemoglobin. Transmission oximetry at wavelengths of 660 and 940 nm and photoplethysmography and rapid signal processing permit reliable and rapid determination of the relative proportion of oxy- and deoxyhemoglobin. 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.

Photoplethysmography permits the measure of arterial hemoglobin saturation by isolating the pulsatile component of the absorbed signal. The peaks and troughs in the blood volume of the finger or ear being transilluminated produce a corresponding pulsatile effect on light absorption, rendering the calculated oxyhemoglobin saturation independent of nonpulsatile venous blood and soft tissue. Calculation of arterial hemoglobin saturation is based on calibration algorithms derived from healthy volunteers. The R values were determined by in vitro measures of oxyhemoglobin saturation and 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 that corresponds to an oxyhemoglobin saturation of approximately 85%.

The pulse oximeter is unable to distinguish other hemoglobin species that absorb light at the emitted wavelengths. Methemoglobin (ferric instead of ferrous hemoglobin) has similar absorption at both 660 and 940 nm with an R value of 1 and a corresponding displayed saturation of 85% regardless of the true value. Carbon monoxide poisoning produces carboxyhemoglobin that has significant absorption at 660 nm and is erroneously interpreted by the pulse oximeter as oxyhemoglobin.

Measurement of Temperature

Profound changes in body temperature during cardiac surgery are common, often deliberate, and affect vital organ function (Fig. 9-5). 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 and decrease systemic oxygen consumption. Hyper- thermia may result from preexisting fever, bacteremia, malignant hyperthermia, or overzealous rewarming during cardiopulmonary bypass.



View larger version (15K):
[in this window]
[in a new window]
?
FIGURE 9-5 Changes in body temperature during hypothermic cardiopulmonary bypass. A brisk diuresis accompanied rewarming, rendering the urine an ultrafiltrate of blood and resulting in the urine (bladder) temperature closely tracking temperature measured in the venous blood in the cardiopulmonary bypass machine.

?
Malignant hyperthermia is a rare inherited disorder of muscle and is potentially fatal.17 It is an autosomal dominant trait with variable penetrance that is almost always quiescent until the patient is exposed to a triggering agent, such as volatile anesthetics or succinylcholine. Malignant hyperthermia is associated with derangements in calcium metabolism. Ineffective uptake of calcium by sarcoplasmic reticulum and abnormal release of calcium from intracellular storage sites occurs with massive skeletal muscle depolarization in response to triggering agents. Clinical manifestations of malignant hyperthermia include increased production of carbon dioxide, tachycardia, and increased cardiac output, followed by fever, metabolic and respiratory acidosis, hyperkalemia, cellular hypoxia, rhabdomyolysis, myoglobinuria, renal failure, and cardiovascular collapse. Serum creatine kinase is increased and may be of diagnostic value. The fever may reach 43?C but may be masked by deliberate hypothermia during cardiopulmonary bypass. Despite increased awareness, improved monitors, and the advent of established treatment algorithms with dantrolene, mortality rates remain high. Treatment is aimed at discontinuing the trigger agent and controlling body temperature through active cooling. Oxygen, hyperventilation, and correction of metabolic acidosis and electrolyte abnormalities are the cornerstone of therapy.

Dantrolene blocks calcium release and is administered at a dose of 2 mg/kg intravenously every 5 minutes for a total dose of 10 mg/kg.18 Intravenous dantrolene is generally continued at 12-hour intervals for a minimum of 24 hours because episodes of malignant hyperthermia may recur even after the trigger agent has been discontinued. The incidence of malignant hyperthermia is approximately 1 in 62,000 anesthetics. Patients with a history of malignant hyperthermia and those with most types of muscular dystrophies are at increased risk. Not all episodes of malignant hyperthermia lead to progressive metabolic and cardiovascular collapse. Unexplained fever after an anesthetic or in the recovery room may identify a patient at increased risk. Testing by in vitro skeletal muscle responses to halothane and/or caffeine is recommended for the preoperative diagnosis of patients suspected to be at increased risk. High-risk patients can be anesthetized safely by using anesthetic drugs such as narcotics, barbiturates, nitrous oxide, local anesthetics, and nondepolarizing muscle relaxants that are not believed to trigger malignant hyperthermia.

Hypothermia after cardiopulmonary bypass is the result of ineffective rewarming, cold operating rooms, cold wet surgical drapes, a large surgical incision, and the administration of cold intravenous fluids. 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.

Temperature is typically monitored from several sites during cardiac surgery. Blood temperature is measured from the tip of the 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 temperature are shell measurements and are impractical.

The degree and site of temperature change 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 is normally 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 due to 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, passage of catheters and pacing electrodes into the heart, 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 easy, reliable insertion, easy 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 the insertion of a central venous catheter for long-term intravenous total parenteral nutrition because of a decreased risk of blood-borne infection.19 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 transducing the pressure waveform prior to the 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 attempts (Fig. 9-6).20



View larger version (74K):
[in this window]
[in a new window]
?
FIGURE 9-6 A two-dimensional short-axis image of the internal jugular vein (IJV) and carotid artery (CA) using a handheld ultrasound transducer.

?
Central venous pressure (CVP) is an index of right ventricular preload. The pulsatile a, c, and v pulse waveforms are a function of uninterrupted return of venous blood to the right atrium, right atrial contraction and right atrial size and compliance, intrathoracic pressure, and mechanical properties of the tricuspid valve and right ventricle. The normal CVP is 6 to 10 mm Hg and is measured at end-exhalation. A decrease in CVP suggests hypovolemia or vasodilation. An increased CVP with normal cardiac function occurs with hypervolemia, vasoconstriction, and increased intrathoracic pressure. CVP is increased by positive pressure ventilation and positive end-expiratory pressure. Systemic hypotension accompanied by an increased CVP suggests cardiac dysfunction. The most common cause of venous hypertension is left-sided heart failure, although acute left ventricular dysfunction may cause an increase in left atrial and pulmonary artery occlusion pressure without significant change in CVP.

Pulmonary artery catheters are inserted via the central venous circulation through the right side of the heart with the catheter tip positioned just downstream to the pulmonic valve. The pulmonary artery catheter measures pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output, and mixed venous oxygen saturation and permits calculation of the derived values of systemic and pulmonary vascular resistance. The pulmonary artery occlusion pressure is an index of left ventricular preload in the absence of mitral stenosis. However, the use of a pressure measurement to estimate preload is limited because of variability in left ventricular size and compliance. The hemodynamic parameters derived from the pulmonary artery catheter may be used to detect myocardial ischemia if ischemia produces ventricular dysfunction that is associated with a decrease in cardiac output, increase in left ventricular end-diastolic pressure, or pulmonary hypertension (Fig. 9-7). However, hemodynamic parameters derived from the pulmonary artery catheter are not as sensitive or as specific for detecting myocardial ischemia as the ECG.21 Pulmonary artery occlusion pressure is affected by volume status, myocardial compliance, mode of ventilation, and ventricular afterload.



View larger version (40K):
[in this window]
[in a new window]
?
FIGURE 9-7 Pulmonary artery occlusion pressure tracing at two time points. The acute onset of myocardial ischemia (B) was associated with ST-segment depression in ECG lead V5, increased pulmonary artery pressures, and a prominent v wave.

?
Complications associated with the insertion of a pulmonary artery catheter include dislodgment of pacemaker wires or right atrial or ventricular clot or tumor, atrial and ventricular arrhythmias, pulmonary infarction, pulmonary artery rupture, catheter entrapment, and heart block. The incidence of right bundle branch block (RBBB) is approximately 3% and may cause complete heart block in patients with a preexisting left bundle branch block (LBBB).22 A mechanism to treat complete heart block (e.g., external pacer) should be available for these patients. The passage of the pulmonary artery catheter can be delayed for most patients until after sternotomy, when heart block can be treated with epicardial pacing wires. Chronic indwelling pulmonary artery catheters are associated with a progressive thrombocytopenia.23 Heparin-bonded catheters decrease the incidence of thrombus formation,24 but high-dose aprotinin may increase the risk of early thrombus formation.25

Multiport pulmonary artery catheters equipped with a tip thermistor permit the measure of pulmonary blood flow or cardiac output by thermodilution. Thermodilution cardiac output is an indicator-dilution technique. The indicator, a known volume of cold saline, is injected rapidly into the right atrium. Cardiac output is calculated from the rate of change in blood temperature in the pulmonary artery over time using the Stewart Hamilton equation26,27:

where CO = cardiac output, V = volume of injectate, TB = blood temperature at time = 0, TI = injectate temperature at time = 0, {Delta} TB(t) is the change in blood temperature at time = t, K1 = density factor, and K2 = 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 does not equal left-sided cardiac output in patients with intracardiac shunts. There are no outcome data to support the routine use of a pulmonary artery catheter in cardiac surgery.

Cardiac output may be monitored continuously using a specialized pulmonary artery catheter. 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. Disadvantages include increased cost and a cardiac output display that is not instantaneous but is an average value over the prior 2 to 10 minutes. Other methods of measuring cardiac output that do not depend on an indwelling pulmonary artery catheter include transthoracic bioimpedance, echocardiography, and analysis of the aortic pressure pulse contour. These have proven cumbersome, impractical, or unreliable for routine use.28

Mixed venous oxygen saturation (Svo2) can be measured intermittently by manual blood sampling from the pulmonary artery or continuously using a modified pulmonary artery catheter equipped with an oximeter. The Svo2 provides a continuous monitor of cardiovascular well-being. Assuming normal oxygen consumption, a normal Svo2 generally denotes adequate oxygen delivery but does not provide information about the adequacy of perfusion to specific organs. A normal Svo2 may not reflect adequate tissue perfusion in patients with intracardiac shunts, sepsis, or liver failure. A decrease in Svo2 is rarely caused by an increase in oxygen consumption during cardiac surgery but is more likely a sign of decreasing oxygen delivery due to decreased cardiac output, anemia, or hypoxia.

Svo2 provides an alternative method to calculate cardiac output if oxygen consumption is assumed to be constant. 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 = oxygen consumption, CO = cardiac output, Cao2 = oxygen content in arterial blood, and Cvo2 = oxygen content in mixed venous blood.

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 (Fig. 9-8). Hypotension associated with increased cardiac output with a normal pulmonary artery occlusion pressure is likely caused by vasodilation and is effectively treated by a vasoconstrictor such as phenylephrine, vasopressin, or norepinephrine. Hypotension associated with a low cardiac output and a low pulmonary artery occlusion pressure indicates hypovolemia and is treated with volume expansion (Fig. 9-9). Hypotension associated with a low cardiac output and increased pulmonary artery and pulmonary artery occlusion pressure indicates cardiac dysfunction and may require treatment with an inotropic or anti-ischemic medication. An insidious decrease in Svo2 may be an early warning of impending circulatory insufficiency due to a decrease in arterial oxygen tension, ventricular dysfunction, bleeding, or tamponade. Svo2 pulmonary artery catheters serve as diagnostic tools and vigilance monitors, especially in the intensive care unit, where early deterioration in cardiac function can be detected and treated before an adverse event occurs.



View larger version (39K):
[in this window]
[in a new window]
?
FIGURE 9-8 Intraoperative hemodynamic recordings showing the time sequence of systemic severe vasodilation (panel A) and catastrophic pulmonary vasoconstrictiontype (panel B) protamine reactions during the reversal of heparin anticoagulation in patients undergoing heart operation. Arterial blood pressure (ABP) and pulmonary artery pressure (PAP) decrease in parallel during systemic vasodilation. In contrast, an increase in PAP and central venous pressure (CVP) precedes the decrease in ABP during the pulmonary vasoconstrictiontype reaction. The decreases in end-tidal carbon dioxide concentration (ETCO2) during the protamine reactions reflect the decrease in blood flow through the lungs.

?


View larger version (21K):
[in this window]
[in a new window]
?
FIGURE 9-9 Decreased left ventricular preload produced by graded estimated blood volume deficits (EBV) was associated with serial decreases in the mixed venous oxygen saturation (Svo2), cardiac stroke volume (SV), left ventricular end-diastolic meridional wall stress (EDWS), left ventricular end-diastolic cavity cross-sectional area (EDA), and pulmonary artery occlusion pressure (PAOP). Patients with dilated cardiomyopathy displayed less change in SV and Svo2 in response to equivalent EBV deficits. *p (Modified with permission from Cheung AT, Weiss SJ, Savino JS: Protamine-induced right-to-left intracardiac shunting. Anesthesiology 1991; 75:904.)

?
Anesthetic Gas Monitors

Inhaled volatile anesthetics are different from other parenteral medications. The dose of the drug administered is dictated by its concentration in the blood rather than by a set standard. The concentration of an anesthetic in the exhaled gas at end-exhalation reflects the alveolar gas concentration that is in direct equilibrium with the blood. Monitoring the concentration of anesthetic in the end-tidal gas mixture adds precision to the administration of inhaled anesthetics and guards against inadvertent overdose.

The concentration of anesthetic gases is measured clinically by mass spectroscopy. A gas sample retrieved from the breathing circuit is analyzed off-line by measuring the dispersion of the ionized sample as it is accelerated and deflected by a magnetic field. The site of impact on a collecting plate is specific for a gas species, and the number of impacts represents the relative concentration of the gas species in the sample. The end-tidal concentration is determined by gating the measure of the anesthetic gas to the carbon dioxide expirogram (capnogram). Other methods of measuring anesthetic and respiratory gases include infrared spectroscopy, Raman spectroscopy, electrochemical and polarographic sensors, and piezoelectric absorption.29

Measurement of Electrolyte Concentration

Electrolyte abnormalities occur commonly during and after cardiopulmonary bypass and are monitored intermittently using routine laboratory tests that are promptly reported to the operating room.30 Reliable on-line measurements of electrolytes are not yet available. The capability to detect and correct electrolyte disturbances is an important aspect of intraoperative care.

Abnormalities in sodium and water homeostasis are caused primarily by hemodilution with solutions used to prime the cardiopulmonary bypass circuit. 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 and does not normally require treatment. Hyperglycemia or excessive mannitol administration causes pseudohyponatremia by decreasing the plasma sodium concentration. Hypernatremia is usually caused by excessive diuresis without free water repletion or by the administration of hypertonic sodium bicarbonate solutions. Hyperkalemia is common because high-potassium cardioplegic solutions 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 is also common during cardiac surgery and may be caused by hemodilution with nonpotassium priming solutions, diuresis, or increased sympathetic tone during nonpulsatile perfusion. Intraoperative hypokalemia is exacerbated by preoperative potassium depletion due to chronic diuretic therapy. Beta2-adrenergic agonists acutely decrease the plasma potassium concentration by directly stimulating cellular uptake of potassium. 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.31,32 Hypocalcemia produces prolongation of the QT interval and T-wave inversions, but significant arrhythmias due 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, in part, explain the gradual increase in ionized calcium concentration to precardiopulmonary bypass levels.33 The etiology of cardiopulmonary bypassinduced hypocalcemia is probably 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.34

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.35,36 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.37

Perioperative glucose control effects outcome after heart surgery. Aggressive protocols aimed at maintaining normoglycemia with the use of insulin infusions during cardiac surgery and into the early postoperative period lead to a decrease in morbidity (e.g., sternal wound infection) and possibly mortality.37,38 However, aggressive control of blood glucose in diabetes increases the incidence of hypoglycemia, which can have severe consequences if not detected early and treated.39

Monitoring the Nervous System

Anesthetics produce characteristic changes in the electrical activity of the brain. The cellular mechanism of general anesthetics is controversial. Unconsciousness and general anesthesia are not achieved by producing energy failure in the brain. The central nervous system cellular concentrations of ATP, ADP, phosphocreatine, glucose, and glycogen are increased and lactate concentrations are decreased during general anesthesia. Most general anesthetics, and especially the extensively studied barbiturates, decrease cerebral metabolic rate and oxygen consumption.

A myriad of neurologic complications may be associated with cardiac surgery,40 including stroke, paralysis, cognitive dysfunction, blindness, and peripheral nerve injury.

STROKE

Stroke associated with cardiac surgery occurs in 3% to 8%41,42 of cases, but the incidence may alarmingly approach 35% to 70% in those with multiple risk factors such as previous stroke, carotid disease, advanced age, hypertension, and diabetes mellitus.41 The majority of strokes are not identified immediately after cardiac surgery, but occur in the first several days postoperatively. The cause of these strokes and their causal relationship to cardiopulmonary bypass remain unclear.

Strokes may be related to micro- or macroemboli but may also be secondary to regional hypoperfusion. The combination of preexisting regional hypoperfusion and embolic phenomenon may be particularly deleterious.43 The existence of a heavily calcified aorta increases the risk of stroke secondary to macroemboli.44 Efforts to reduce the incidence of stroke in this patient group include the use of "off-pump" coronary artery bypass grafting, epiaortic ultrasound to identify "safe" areas for cannulation, and single clamping techniques for proximal anastamoses.45 Previous work in animal models has demonstrated that in regions of the brain with compromised blood flow, acute anemia may not be well tolerated.46 Acute anemia in individuals at risk for cerebrovascular disease may be exacerbated by an imbalance in oxygen supply and demand.47

The possibility exists to intervene to alter the course of perioperative stroke in individuals at high risk. For example, the application of intra-arterial thrombolytics in a highly selective fashion to the affected cerebral arteries can be done with acceptable morbidity even early after cardiac surgery.48,49

PARALYSIS

Paralysis, a devastating complication, is associated with dissection of the thoracic aorta, with repair of descending thoracic and thoracoabdominal aneurysm, and most recently after placement of endovascular stents.50 The incidence in repair of a descending thoracic or thoracoabdominal aneurysm is 5% to 10%51,52 and may exceed 25% in certain high-risk groups.53 The likely cause is hypoperfusion of the spinal cord during aortic cross-clamping and ligation of intercostal and lumbar arteries.54 Risk factors for paralysis include extent of the aneurysm and acuteness of disease. Those subjects without demonstrated flow in intercostals within the aneurysm may be at lower risk for paralysis after resection,55 presumably because collateral blood supply to the cord in the involved region has been allowed to slowly occur, while subjects experiencing acute dissection, which does not permit time for collateralization, may experience a high rate of paralysis.

Intraoperative monitoring including motor evoked potentials and somatosensory potentials may be of some benefit to detect early spinal cord ischemia56,57 yet may lack the sensitivity and specificity necessary to reliably guide intervention.58 Preemptive measures to limit the degree of spinal cord ischemia have included identification and reimplantation of the artery of Adamkiewicz as well as intercostal vessels,59,60 placement of cerebrospinal fluid (CSF) drainage catheters to increase the mean arterial pressure to CSF pressure gradient, epidural cooling of the spinal cord,61,62 and distal perfusion techniques such as left atrial-femoral artery (LA-FA) bypass to enhance cord perfusion from below the inferior clamp site.63,64 All of the above techniques have met with potentially important but limited success and controlled studies demonstrating a difference in outcome do not exist.65 Recent work has emphasized the importance of addressing spinal cord ischemia in a similar fashion to the management of coronary or cerebral ischemia.66 A continuum of injury exists from infarcted to ischemic tissue.

Signs of spinal cord ischemia may improve or deteriorate with time and there may be, at the very least, an opportunity to ameliorate the extent of the injury through early intervention, such as increasing perfusion pressure and decreasing CSF pressure through drainage.67 Most treatments are fraught with risk (e.g., the placement of CSF drainage catheters).68

COGNITIVE DYSFUNCTION

Postoperative alterations in cognitive function include disturbances of memory, attention, and intellectual function. Cognitive dysfunction occurs after cardiac operations at a rate estimated as high as 80% in the acute phase after surgery and may persist in 20% to 40% of cases depending on length of follow-up.69 More than any other factor, advanced age has been consistently identified as the greatest risk factor for cognitive dysfunction after cardiac surgery with cardiopulmonary bypass. Early and late mortality may be markedly increased, quality of life is diminished, and costs of care are increased in the short and long run.70

Etiology has focused upon a myriad of potential causes71 that predominantly include the effects of cardiopulmonary bypass such as hypotension,72 microemboli,73 open versus closed cardiac procedures,74 acute anemia,75 changes in brain water content,76 hypoxemia, rewarming strategies,77 cold versus warm cardiopulmonary bypass,78 pH management strategy (alpha-stat vs. pH-stat),79 pulsatile versus nonpulsatile perfusion,80 bypass duration,81 flow rates,82 hypo- and hyperglycemia,83 presence of the apolipoprotein E in-4 allele,84 and immunologic mechanisms.85 Lastly, although cognitive dysfunction in the general population has been associated with chronic hypotension86 and congestive heart failure,87 the role of left ventricular function in cognition surrounding cardiac surgery is not known.

Research outside the arena of cardiac surgery into neurologic injury in cerebrovascular disease has focused upon the immune system as the generator of mediators and modulators of the cerebral endothelium88,89 and of blood-brain barrier permeability.90 One theory of immunologic mediated neuronal injury postulates a cascade of events initiated by complement- and neutrophil-mediated vascular endothelial damage and disruption of the blood-brain barrier, thus allowing neutrophil access to the parenchyma with resultant neural destruction.88,90

NEUROLOGIC SEQUELAE IN NONCARDIAC SURGERY

It would be irresponsible not to mention that stroke and cognitive dysfunction occur in patients after noncardiac surgery at a rate that is significantly less than that which is seen in the cardiac surgery group, yet the incidence is not negligible,9193 and may also be associated with prolonged deficits.94,95 There may be similar risk factors and similar pathophysiologic mechanisms in this group of patients, especially in the origins of delayed stroke in the perioperative period. Investigations may ultimately even implicate the anesthetic agents themselves,96 irrespective of issues of intraoperative hemodynamic management.

Neurophysiological monitoring techniques permit assessment of nervous system function during and early after operation because clinical evaluation is not possible. Techniques to monitor neurophysiological function during general anesthesia include electroencephalography (EEG) and somatosensory evoked potentials (SSEP). The EEG is a recording of the spontaneous electrical activity of the cerebral cortex and is defined by frequency, amplitude, and spatial distribution.97 The amplitude of electrical activity decreases by more than 80% when the recording electrode is displaced only 2 cm from the site of maximum amplitude. This necessitates multiple electrodes and channel recordings to obtain a spatial representation of the EEG rhythm.98 A change in EEG amplitude or frequency may be produced by cerebral ischemia, anesthetics, or hypothermia. Barbiturates produce a flat EEG, whereas enflurane may cause seizurelike activity. EEG burst suppression is not uncommon after induction of general anesthesia but does not exclude an impending neurologic catastrophe if induced by changes in cerebral blood flow. While continuous EEG monitoring may detect cerebral ischemia during carotid operations, its application during cardiac operations is problematic because the decrease in EEG frequency and amplitude due to anesthesia and hypothermia during operation cannot be distinguished from changes caused by cerebral ischemia.99,100 Electrical artifacts from the heart-lung machine also interfere with the ability to continuously monitor the EEG during operation. Intraoperative monitoring of SSEP to detect cerebral ischemia overcomes some of the problems inherent to EEG monitoring because the temperature dependency of SSEP is well established.101 Embolic stroke and brachial plexus injury65,66 can be detected using intraoperative SSEP monitoring, but the utility, sensitivity, and specificity of this technique for detecting, preventing, and guiding the treatment of neurologic complications remain to be established (Fig. 9-10).102,103



View larger version (21K):
[in this window]
[in a new window]
?
FIGURE 9-10 Intraoperative monitoring of somatosensory evoked potentials (SEPs) was used for the acute detection of embolic stroke during mitral valve replacement. The symmetric changes in the peak-to-peak amplitudes of N20-P22 SEPs before removal of the aortic cross-clamp were caused by the decrease in body temperature during deliberate hypothermia. The asymmetric decrease in the right cortical SEPs after removal of the aortic cross-clamp was associated with an acute embolic stroke to the right thalamus or right somatosensory cortex. CPB = cardiopulmonary bypass; NP = nasopharyngeal temperature; X-clamp = ascending aorta cross-clamp. (Reproduced with permission from Cheung AT, Savino JS, Weiss SJ, et al: Detection of acute embolic stroke during mitral valve replacement using somatosensory evoked potential monitoring. Anesthesiology 1995; 83:201.)

?
Alternatively, intraoperative transesophageal echocardiography (TEE) and transcranial Doppler (TCD) may be used to detect arterial embolic events (Fig. 9-11). The embolic burden to the cerebral circulation measured by quantitative TCD correlates with the incidence of intraoperative surgical manipulation and postoperative neurologic deficits.104 Intraoperative TEE can be applied to detect right-to-left intracardiac shunting through an atrial septal defect,105,106 intracardiac masses,107,108 or residual air within the cardiac chambers.109 Routine epiaortic ultrasonography to assess the degree of aortic atherosclerosis and guide the insertion of the aortic cannula and application of the aortic cross-clamp may decrease the risk of embolic stroke, but outcome data to suggest efficacy are sparse.110



View larger version (104K):
[in this window]
[in a new window]
?
FIGURE 9-11 Middle cerebral artery blood flow velocity measured intraoperatively using a 2-MHz transcranial Doppler ultrasound transducer. The phasic velocity profile in the top panel was recorded before cardiopulmonary bypass. The irregular high-velocity, high-amplitude signals recorded in the lower panel indicate microemboli traveling through the middle cerebral artery immediately after ventricular ejection.

?

?? ANESTHESIA
 Top
 Previous
 Next
 References
?
Anesthetic techniques presently employed for patients undergoing cardiac operations have been selected after extensive testing and clinical experience. Current clinical practice techniques have minimal organ toxicity, predictable cardiovascular and physiological effects, well-established pharmacokinetic behavior, and excellent safety profiles. No benchmark anesthetic technique has been defined for all patients undergoing cardiac operations.111114 Combining drugs that selectively provide hypnosis, amnesia, analgesia, and muscle relaxation permits control of the anesthetic state and minimizes side effects of a single anesthetic drug used in high concentrations. Achieving the desired anesthetic state while preserving or improving vital organ function during operation requires an understanding of the physiological actions of anesthetics, individually and in combination, in patients with a wide range of medical conditions.

Anesthesia drug management is dictated, in part, by the underlying cardiovascular disorder. Coronary artery disease renders the ventricle susceptible to myocardial ischemia, and management is designed to support coronary perfusion pressure while decreasing myocardial oxygen demands. Tachycardia, hypertension, and increased inotropic state caused by nociception during operation are prevented by anticipating the inciting events and providing effective anesthesia. In contrast, patients with heart failure due to valvular disease, dilated cardiomyopathy, or cardiac tamponade may be dependent on underlying sympathetic tone to support the circulation. In these patients, the anesthetist must be prepared to pharmacologically replace endogenous catecholamines while the patient is anesthetized.

Anesthetic-induced hemodynamic perturbations must be considered when assessing valve function intraoperatively using TEE (Fig. 9-12). Patients with regurgitant valve lesions frequently exhibit acute hemodynamic improvement during anesthesia because systemic oxygen demand and ventricular afterload decrease with anesthetic agents. Potent volatile anesthetics produce varying degrees of dose-dependent vasodilation and afterload reduction: isoflurane > enflurane > halothane. Assessment of mitral regurgitant grade during general anesthesia is not necessarily predictive of regurgitant grade in the awake state and may lead to mismanagement.115,116 Provocative pharmacological testing may be required to mimic circulatory conditions in the awake, exercising patient. Stress-testing the mitral valve may be achieved with incremental doses of phenylephrine to increase the transmitral systolic pressure gradient; however, the determinants of regurgitant volume are many, and it is unlikely that phenylephrine reliably reproduces the cardiovascular conditions that occur when a patient is exercising.



View larger version (129K):
[in this window]
[in a new window]
?
FIGURE 9-12 The relationship of increasing doses of isoflurane to the magnitude of mitral regurgitation and pulmonary artery pressures. The systemic unloading effects of isoflurane decreased mitral regurgitation from moderate to mild and decreased pulmonary artery pressures almost to normal.

?
Maintenance of cardiovascular stability during general anesthesia for patients with aortic stenosis is based on avoiding systemic vasodilation and tachycardia and preserving sinus rhythm. Systemic vasodilation provides no significant decrease in left ventricular afterload because of the stenotic aortic valve. Tachycardia is poorly tolerated due to shortened diastole and decreased filling of the noncompliant left ventricle. Nonsynchronous atrial contraction, a common occurrence during induction of general anesthesia, may produce significant hypotension and rapid deterioration in stroke volume. Narcotic-based anesthetics possess many desired hemodynamic attributes for patients with aortic stenosis. Synthetic narcotics are potent vagotonic drugs that decrease heart rate with minimal vasodilating effects and provide profound analgesia.

Anesthetics and Neuromuscular Blockers

INHALED ANESTHETICS

Inhaled anesthetics alone produce all the conditions necessary for operation.117 All inhaled anesthetics cause circulatory depression at concentrations necessary to produce general anesthesia. When ventilation is controlled, circulatory actions of the inhaled anesthetics usually limit the anesthetic dose that can be tolerated, especially in patients with cardiovascular disease. For this reason, lower doses of inhaled anesthetics are usually combined with other anesthetics to produce general anesthesia 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. 9-13).118120 Inhalation anesthetics produce a dose-dependent decrease in mean maximal velocity of circumferential shortening, mean maximal developed force, and dP/dt.121123 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. The decrease in blood pressure in response to 1.0 minimum alveolar concentration (MAC) of halothane is primarily the result of decreased cardiac output caused by direct myocardial depression. Despite a decrease in myocardial contractility, cardiac output is generally 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. 9-14).124 Halothane, enflurane, 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. 9-15). Experimental studies suggest these agents cause minimal changes in left ventricular diastolic compliance but impair left ventricular diastolic relaxation in a dose-dependent manner.125 These agents have minimal direct effects on left ventricular preload. Left and right ventricular end-diastolic pressures may increase during anesthesia because of impaired diastolic filling and decreased cardiac output. Halothane and enflurane are the most potent direct myocardial depressants, followed by isoflurane, desflurane, and sevoflurane.



View larger version (39K):
[in this window]
[in a new window]
?
FIGURE 9-13 The actions of inhaled anesthetics on left ventricular myocardial segment shortening as measured in chronically instrumented dogs with an intact and blocked autonomic nervous system (ANS). All inhaled anesthetics caused a significant decrease in segment shortening at both 1.25 and 1.75 MAC in comparison with awake animals. (Reproduced with permission from Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, and enflurane in the chronically instrumented dog. Anesthesiology 1991; 74:539.)

?


View larger version (25K):
[in this window]
[in a new window]
?
FIGURE 9-14 Dose-dependent changes in mean arterial pressure, heart rate, cardiac index, and systemic vascular resistance produced by halothane, isoflurane, and desflurane in normocarbic adults. Despite the myocardial depressant effects of isoflurane and desflurane, cardiac output is maintained during anesthesia with these agents in part because of a decrease in left ventricular afterload and increase in heart rate. (Data from Weiskopf RB, Cahalan MK, Eger EI 2nd, et al: Cardiovascular actions of desflurane in normocarbic volunteers. Anesth Analg 1991; 73:143. Used with permission.)

?


View larger version (18K):
[in this window]
[in a new window]
?
FIGURE 9-15 Dose-dependent changes in central venous pressure produced by halothane, isoflurane, and desflurane in normocarbic adults. (Data from Weiskopf RB, Cahalan MK, Eger EI 2nd, et al: Cardiovascular actions of desflurane in normocarbic volunteers. Anesth Analg 1991; 73:143. Used with permission.)

?
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 compared with normal myocardium. In contrast, sympathetic nervous system activation due to nociception may mask clinical signs of circulatory depression caused by inhaled anesthetics. Cardiodepressants and adrenergic antagonists potentiate the cardiovascular depressant actions of inhaled anesthetics.

The administration of inhaled anesthetics in patients with preexisting cardiovascular diseases has potential advantages. The myocardial depressant and arterial vasodilating actions of anesthetics benefit patients with coronary insufficiency if perfusion pressure is maintained. The negative inotropic properties of inhalation anesthetics decrease myocardial oxygen demand and may create a more favorable myocardial oxygen balance. The vasodilating and antihypertensive actions of anesthetics effectively control an increase in blood pressure in response to surgical pain, but anesthetic-induced hypotension may reduce coronary perfusion pressure and coronary blood flow.

Enflurane is a mild coronary vasodilator, while halothane has little effect on coronary vascular tone. Regional wall motion abnormalities and ECG evidence of myocardial ischemia associated with enflurane or halothane are due to decreases in coronary perfusion pressure rather than to a redistribution of myocardial blood flow.126,127 Isoflurane causes endothelium-dependent inhibition of the contractile response of canine coronary arteries.128 The direct coronary artery vasodilating action of isoflurane may increase coronary blood flow but also may increase the risk of myocardial ischemia in patients with steal-prone coronary anatomy by attenuating autoregulation of coronary blood flow. Coronary anatomy associated with isoflurane-induced coronary steal is a total occlusion of a major coronary branch and a hemodynamically significant (greater than 50%) stenosis in the artery that supplies the collateral-dependent myocardium. The proposed mechanism is vasodilation and a decrease in coronary perfusion pressure downstream to the stenosis that decreases blood flow through the high-resistance, less-responsive collateral network.129 However, there is no convincing clinical evidence that isoflurane should be avoided in patients with coronary artery disease any more than other nonselective coronary vasodilators (e.g., nitroprusside).130 The increase in heart rate and sympathetic tone associated with isoflurane and desflurane increases oxygen demand by producing tachycardia and may cause myocardial ischemia in susceptible patients. This is more important than the theoretical risk of coronary steal.131133

Volatile anesthetics have anti-ischemic, preconditioning properties resulting in cardioprotection against myocardial infarction via KATP channels.134 Isoflurane, desflurane, and sevoflurane have cardioprotective properties independent from anesthetic improvement of myocardial oxygen supply demand balance.135 However, there are no clinical outcome data to suggest that anesthetized patients with coronary artery disease fare better with the use of volatile anesthetics compared to intravenous agents.

Halothane sensitizes the myocardium to epinephrine-induced ventricular dysrhythmias and may be problematic in patients at risk for ventricular tachycardia, especially if sympathomimetics are given concurrently. The subcutaneous dose of epinephrine required to cause ventricular premature contractions during anesthesia with isoflurane, enflurane, or desflurane is approximately 4-fold greater than the dose required during halothane anesthesia.136,137 The susceptibility to catecholamine-induced dysrhythmias is exacerbated by hypercarbia.

Junctional rhythms are observed often with all inhaled anesthetics but most commonly with enflurane. The loss of atrial augmentation of ventricular preload with a junctional rhythm contributes to a decrease in blood pressure during inhalation anesthesia. Junctional rhythms are frequently problematic in patients with aortic stenosis and left ventricular hypertrophy who have poor ventricular diastolic compliance. Junctional rhythms can be treated with transesophageal, transvenous, or direct atrial pacing, decreasing the dose of inhalation anesthetic, or administering an anticholinergic drug such as glycopyrrolate or atropine.

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 (brain, heart, kidneys) and a decrease in blood flow to skin, muscle, and the gastrointestinal system. Volatile inhalation anesthetics impair this protective response and compromise vital organ perfusion if administered in high doses during periods of circulatory shock.

Nitrous oxide (N2O) is also an inhaled anesthetic but not potent enough to be used alone for general anesthesia. It is often used with other anesthetics because it decreases the MAC of halothane and isoflurane. N2O is rarely used during cardiac operations because it diffuses into and expands the volume of gas-containing cavities and may increase the size of arterial gas emboli.

Rare cases of acute postoperative hepatic necrosis have been attributed to halothane administration.138 Although the epidemiologic evidence implicating halothane as the cause of this syndrome remains controversial, the incidence of this idiosyncratic reaction is estimated in the range of 1 in 10,000 to 1 in 35,000 halothane anesthetics. Repeated exposures to halothane, reduced splanchnic blood flow, obesity, hypoxemia, enhanced reductive metabolism of the drug, and increased levels of hepatic enzymes induced by chronic drug use, malnutrition, and underlying liver disease appear to be risk factors for postoperative hepatitis. The perceived risk of halothane-induced hepatitis has favored increased use of newer anesthetic agents such as enflurane, isoflurane, and desflurane. Sevoflurane, a newer generation ether volatile agent, offers lack of airway reactivity, nonpungent odor, low flammability, rapid induction and emergence, and minimal cardiovascular and respiratory side effects.139,140 The accumulation of Compound A, a potential renal toxin and byproduct of sevoflurane use, has been associated only with low fresh gas flow (These newer agents undergo minimal hepatic metabolism, do not decrease hepatic blood flow, and have not been implicated in anesthetic-induced liver dysfunction.

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 closely controlled.113,137

SEDATIVE-HYPNOTICS

Sedative-hypnotics are a broad class of anesthetic drugs that includes barbiturates, benzodiazepines, etomidate, propofol, and ketamine. They are used for preoperative sedation, 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 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.141 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.142,143 The decrease in arterial pressure after propofol administration is attributed primarily to arterial and venous dilatation.144,145 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 an nonintubated patient requires the presence of an anesthesiologist because respiratory depression is common. Etomidate and ketamine are administrated for rapid induction of general anesthesia in patients with preexisting hemodynamic compromise because they generally cause little or no change in circulatory parameters.146 These agents are useful for unstable patients undergoing emergency operation, reexploration for bleeding, or cardioversion. Etomidate has virtually no effect on myocardial contractility even in diseased ventricular muscle.147,148 However, etomidate inhibits adrenal synthesis of cortisol by blocking beta hydroxylase and therefore is limited to short-term use as an intravenous anesthetic induction agent. Ketamine often increases heart rate and blood pressure after anesthetic induction because it maintains sympathetic tone.149 The direct negative inotropic and vasodilating effects of ketamine can be unmasked when it is administered to critically ill patients with catecholamine depletion.150 Ketamine is not used routinely because it may cause postoperative delirium, especially if it is administered in the absence of other sedative-hypnotics.

Centrally acting alpha2-adrenergic agonists such as clonidine possess sedative and analgesic actions but do not produce anesthesia. Preoperative administration of clonidine to cardiac surgical patients decreases narcotic requirements and improves hemodynamic stability during operation.151 Alpha2 agonists are potent sympatholytic agents and also may be effective at attenuating sympathetically mediated myocardial ischemia.152 Dexmedetomidine is a highly selective intravenous alpha2-adrenergic agonist with sedative actions.153 Dexmedetomidine administered at a rate of 0.2 to 0.7 ?g/kg/h intravenously provides effective postoperative sedation for intubated cardiac surgical patients and decreases the need for narcotic analgesics by approximately 50%. Because alpha2-adrenergic agonists have little or no respiratory depressant actions, weaning from mechanical ventilatory support and tracheal extubation can be accomplished without interruption of the dexmedetomidine infusion. The most common adverse effects of dexmedetomidine are hypotension and bradycardia. At dexmedetomidine doses greater than 1.0 ?g/kg/h, arterial pressure may increase due to direct activation of the alpha2B receptor subtype, which produces peripheral vasoconstriction. Dexmedetomine-induced vasoconstriction causes an increase in systemic vascular resistance, an increase in pulmonary vascular resistance, and a decrease in cardiac output.

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. The three types of opioid receptors most studied are the mu, delta, and kappa receptors. Mu receptors are densely concentrated in the neocortex, brainstem, and regions of the central nervous system associated with nociception and sensorimotor integration.154 Two different mu receptor subtypes produce analgesia and respiratory depression, leading to the possible development of selective agonist or antagonist compounds.

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 is critically ill and dependent on endogenous catecholamines (e.g., those with 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 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.156 The rigidity usually affects the thoracic and abdominal musculature and is commonly observed with doses of narcotic used in cardiac anesthesia. Myoclonic activity often associated with muscle rigidity can easily be mistaken for grand mal seizures. There is no evidence that opioids induce seizures when there is adequate oxygenation and ventilation.157 Opioid-induced muscle rigidity is immediately reversed by the administration of neuromuscular blockers.

The nonselective opioid antagonist naloxone reverses narcotic-induced respiratory depression. Narcotic antagonists must be titrated carefully to effect. Sudden reversal of opioid-mediated analgesia may produce systemic and pulmonary hypertension and tachycardia and is potentially life-threatening for patients with coronary artery disease.158 The reversing effect of naloxone on narcotic-induced respiratory depression is significantly shorter than the respiratory depressant effects of most opioids, except for ultrashort-acting synthetic narcotics (e.g., alfentanil, remifentanil). A patient who receives a single intravenous dose of naloxone is susceptible to renarcotization after initial reversal of respiratory depression. For this reason, the initial bolus dose of naloxone is typically followed by an intramuscular injection or intravenous infusion, and patients are monitored closely. Longer acting opioid antagonists include nalmefene, which has an elimination half-life (t1/2B) of 8.5 hours, in contrast with the t1/2B of 1.5 hours for naloxone.159 Mixed opioid agonists-antagonists (e.g., nalbuphine) may decrease the risk of hypertension, tachycardia, and dysrhythmias but do not reverse respiratory depression as reliably as naloxone.160

Opioid tolerance is a decrease in response (both analgesia and respiratory depression) to a narcotic due to prior exposure. Tachyphylaxis is the rapid development of drug tolerance. 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.155 Perioperative exposure to morphine and synthetic narcotics is unlikely to produce the downregulation and desensitization of opioid receptors believed necessary for narcotic dependence.161 Acute tolerance to fentanyl in humans is likely to occur only after prolonged infusion and to a lesser extent in the perioperative period. Cardiac surgical patients receiving narcotic infusions in the intensive care unit develop tolerance and require increasing doses to sustain the desired effect.162

The synthetic narcotics such as fentanyl, sufentanil, and alfentanil overcome some of the problems of morphine-based anesthetics because of increased lipid solubility, more rapid onset of action, increased anesthetic potency, absence of histamine release, and independence of renal function for drug clearance. Development of short-acting narcotic anesthetics also may improve the ability to control anesthetic depth without prolonging recovery time. Ultrashort-acting narcotics (e.g., remifentanil) may have a unique niche in cardiac anesthesia because their effect is terminated almost immediately on stopping the drug infusion due to rapid in vivo ester hydrolysis.163 Other side effects of narcotics include pruritus, nausea, constipation, and urinary retention.

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 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 at the motor end plate. Succinylcholine is an acetycholine 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 9-3). The newer neuromuscular blocking drugs such as vecuronium, cis-atracurium, doxacurium, and rocuronium have virtually no cardiovascular side effects and are not dependent on renal function for elimination. Metocurine and gallamine are completely dependent on renal function for elimination and are infrequently used in clinical practice. 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. The neuromuscular blockers D-tubocurarine, metocurine, mivacurium, and atracurium may decrease blood pressure and increase heart rate indirectly by mediating release of histamine. The cardiovascular effects of these neuromuscular blockers may be attenuated by pretreatment with H1- and H2-receptor antagonists. Long-term administration of vecuronium is associated with development of myopathy in patients on glucocorticoid therapy.164


View this table:
[in this window]
[in a new window]
?
TABLE 9-3 Neuromuscular blocking drugs

?
Discontinuing general anesthesia or sedation before complete recovery from neuromuscular blockade is very distressing for a patient 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 acetylcholine-esterase 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 due to the non-antagonized parasympathetic activity associated with acetylcholinesterase inhibitors in the denervated heart.165 Reliable reversal of neuromuscular blockade with cholinesterase inhibitors is usually achieved only after muscle strength has recovered spontaneously to approximately 25% of baseline levels. Recovery of neuromuscular function is measured by a train-of-four twitch monitor applied to the ulnar nerve.

LOCAL ANESTHETICS

Local anesthetic drugs block the propagation of action potentials in electrically excitable tissue. 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 is often added to local anesthetic solutions to prolong the anesthetic duration, but may cause tachycardia or cardiac arrhythmias when absorbed into the systemic circulation. Inadvertent intravascular injection of a local anesthetic may cause seizures, myocardial depression, hypotension, bradycardia, ventricular arrhythmias, or even cardiac arrest. Among the local anesthetics, bupivacaine has the greatest potential for cardiac toxicity. Ropivacaine is less cardiotoxic than bupivacaine.166,167

Special Anesthetic Techniques

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. Anesthesia is often necessary to facilitate tracheal intubation; however, the effects of general anesthetics on respiratory and circulatory function typically produce respiratory depression and may cause apnea, instability of the patient's airway, aspiration pneumonitis, hypoxia, hypercarbia, and cardiovascular collapse. 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.168 The difficult airway (e.g., Mallampati class 4) often can be intubated with the patient in a sedated state 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. Other techniques include mask ventilation, laryngeal mask ventilation, esophageal-tracheal combitube ventilation, blind oral or nasal intubation, direct laryngoscopy, rigid ventilating bronchoscopy, light wand intubation, retrograde intubation, transtracheal jet ventilation, cricothyroidotomy, and tracheostomy.

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, thoracic aortic operations, 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. 9-16) or bronchial blockers (Fig. 9-17).



View larger version (36K):
[in this window]
[in a new window]
?
FIGURE 9-16 (A) Right-sided double-lumen endobronchial tube positioned such that Murphy's eye is aligned with the orifice of the right upper lobe bronchus. Indications for a right-sided tube are surgery involving the left main-stem bronchus, patients with a prior left pneumonectomy, stenosis, compression, or mass in the left main bronchus, and circumstances in which the trachea needs to be protected from soilage from contents in the right lung (e.g., abscess). (B) Left-sided double-lumen endobronchial tube.

?


View larger version (38K):
[in this window]
[in a new window]
?
FIGURE 9-17 Bronchial blockers permit single-lung ventilation but do not permit suctioning or rapid deflation of the nonventilated lung. Position of the bronchial blocker is less stable compared with a double-lumen endobronchial tube.

?
Wire-guided bronchial blocker kits often contain an adapter for a standard endotracheal tube with 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. Bronchial blockers for lung isolation are preferred when the larynx is too small to accommodate a double lumen endobronchial tube (rare in the adult patient), when it is difficult or dangerous to change an existing endotracheal tube, or when the tracheal or mainstem bronchus is distorted by a mediastinal mass or aortic aneurysm.

The routine use of fiberoptic bronchoscopy has decreased the complication rates and eliminated uncertainty regarding positioning of these devices in the airway. Hypoxemia caused by transpulmonary shunt through the nonventilated lung during single-lung ventilation often requires modification of the anesthetic technique to preserve hypoxic pulmonary vasoconstriction.

REGIONAL ANESTHESIA AND ANALGESIA

Epidural or intrathecal administration of local anesthetics and narcotics can provide profound postoperative analgesia after thoracic and major abdominal operations with less sedation or respiratory depression compared to parenteral narcotic analgesia.169171 However, the risk of hematoma in the spinal canal during or after cardiopulmonary bypass and heparinization has limited the use of epidurals for cardiac surgery. Patient-controlled epidural analgesia using infusion pumps can be triggered by patient demand with a predetermined maximum lockout dose to prevent overdose. Patient-controlled epidural analgesia is an effective method to titrate the dose of epidural local anesthetic and 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.172

The epidural catheter is most often inserted prior to operation before systemic anticoagulation. Instrumentation of the epidural space for insertion of the catheter or removal of the epidural catheter is contraindicated in anticoagulated patients and in patients with coagulopathy because of the risk of epidural hematoma formation.173,174 Epidural analgesia is provided by administering a continuous infusion of dilute solution of local anesthetic or narcotic, or a combination of the two, into the epidural catheter (e.g., bupivacaine 0.05% and fentanyl 2 ?g/mL at a rate of 4 to 8 mL per hour).

The most common side effect of epidural analgesia is hypotension caused by local anesthetic blockade of the preganglionic vasomotor efferents of the sympathetic nervous system and loss of compensatory vasoconstriction. This side effect can be decreased by decreasing the concentration of the local anesthetic relative to the narcotic analgesic used in the epidural infusion. Respiratory depression can also occur with systemic absorption of the narcotic. The onset of respiratory depression is sometimes delayed or unpredictable. Nausea and pruritis are also common side effects of epidural or intrathecal narcotics. Epidural hematoma formation causing spinal cord compression is a rare, but potentially catastrophic complication of epidural and intrathecal analgesia, with an estimated frequency of 1 in 150,000 cases.175

Thoracic epidural anesthesia has been employed successfully for treatment of refractory angina.176,177 Selective anesthesia of T1 to T5 thoracic dermatomes with epidural local anesthetic inhibits sympathetic innervation of the heart and regional vasculature. Thoracic epidural anesthesia decreases left ventricular contractility and heart rate while prolonging phase IV of the cardiac action potential.178 The decrease in myocardial oxygen consumption, reduced arrhythmogenicity, and increase in diameter of the stenotic coronary arteries are the proposed mechanisms for the abolition of chest pain in unstable angina patients who receive thoracic epidural local anesthetic.179183 With exercise testing, these patients have a smaller ischemic burden (less ST-segment depression) for a given workload with epidural anesthesia compared with control exercise without epidural anesthesia. Treatment of myocardial ischemia with an infusion of local anesthetics or opioids into the epidural space is not without risk in patients who are likely to receive anticoagulants and/or thrombolytics and who may have significant preexisting left ventricular dysfunction.

CONTROLLING LUMBAR CEREBROSPINAL FLUID PRESSURE

Several studies and clinical experience suggest that spinal fluid drainage may improve neurologic outcome from spinal cord ischemia during thoracoabdominal aortic operations.183186 Although the clinical efficacy of lumbar CSF drainage remains controversial, the technique is routine at some institutions.187188 CSF drainage and a decrease in the lumbar CSF pressure can be achieved by aseptically inserting a subarachnoid catheter through a Tuohy needle positioned in a lower lumbar vertebral interspace. The catheter is typically inserted 1 to 2 hours before systemic anticoagulation with the patient in a lateral decubitus position. CSF is passively drained to reduce lumbar CSF pressure to approximately 10 to 12 mm Hg during operation. Reducing CSF pressure further may cause an abducens nerve palsy and postoperative diplopia. The catheter is secured and CSF drainage continued typically for 24 hours after operation. In the absence of spinal cord ischemia, the catheter is capped at 24 hours after operation and removed at 48 hours after operation. 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 successfully reverse delayed-onset paraplegia or paraparesis in some patients after thoracic aortic reconstruction.189 Complications associated with lumbar CSF catheters include meningitis, persistent CSF leak, breakage and retention of a catheter fragments, and epidural hematoma. The risk of epidural hematoma is increased when the CSF catheter is inserted or removed in anticoagulated patients.


?? THE CONDUCT OF ANESTHESIA, SURGERY, NURSING, AND PERFUSION
 Top
 Previous
 Next
 References
?
Cardiac surgery is conducted in an interdisciplinary environment among surgeon, anesthesiologist, perfusionist, and nursing staff. The operating room requires a minimum of 800 sq ft to comfortably accommodate the patient, health care providers, standard operating room equipment, cell saver, heart-lung machine, and assist devices, if needed.190 The required square footage may be greater for the higher technology procedures such as robotic surgery.

The anesthetic begins before the patient arrives in the operating room. Patients are premedicated with a sedative-hypnotic (e.g., scopolamine, benzodiazepine) and analgesic (e.g., morphine) unless the associated mild degree of respiratory depression is unwarranted. The patient's identification and scheduled procedure are verified immediately on arrival in the operating room. The patient is escorted into the operating room and placed onto the operating table, and routine noninvasive monitors are applied. 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 6 hours prior to induction of general anesthesia. Prophylactic antibiotics are administered after insertion of an intravenous catheter. A catheter is inserted 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 commonly used to provide measures of cardiac output and estimate ventricular filling pressures.191 Large-bore intravenous catheters are inserted for patients who are undergoing reoperation because of the possibility of rapid blood loss during sternotomy. The immediate availability of typed and crossmatched blood is verified before skin incision. Patients undergoing reoperations are more likely to have a positive antibody screen that delays the availability of blood products. External defibrillation pads are always applied to patients undergoing reoperation or in procedures in which access to the heart with internal paddles is not readily available.

Anesthesia care begins in the preinduction period, documents significant events of surgery, and becomes part of the patient's medical record. Prior to induction of general anesthesia, a baseline set of hemodynamic measurements is obtained and recorded. These measures often guide the choice of anesthetic drugs and technique, provide a baseline for comparison later, and confirm hemodynamic data acquired during cardiac catheterization. Automated record keepers eventually may relieve the anesthetist of recording this data.

Induction of general anesthesia is achieved by inhalation of volatile potent anesthetics, the intravenous administration of sedative-hypnotics, or both. 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 used commonly 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. Laryngoscopy is extremely stimulating (painful) and, if the patient is inadequately anesthetized, causes severe hypertension and tachycardia and stimulates vasovagal reflexes. The inability to ventilate or intubate the trachea in a patient after the induction of general anesthesia is a medical crisis and may require transtracheal jet ventilation, cricothyroidotomy, or tracheostomy. Patients with a history of a technically difficult tracheal intubation, poor dentition, large tongue, limited mouth opening, inability to sublux the mandible, or a recessed chin are at increased risk of airway complications, and it may be prudent to secure the airway while they are still awake. Successful intubation of the trachea is verified by the appearance of a carbon dioxide expirogram. 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 prior to surgical preparation and draping. Regions susceptible to pressure injuries are protected and padded.

Maintenance of general anesthesia is achieved by continuous or intermittent administration of anesthetic drugs titrated to effect while monitoring the conduct of operation and vital physiological functions. Short-acting vasoactive agents with rapid onset of action are usually preferred for controlling the circulation because conditions constantly change. The cardiovascular actions of inhaled anesthetics are often utilized for short-term blood pressure control because effective concentrations can be reached quickly and monitored in real time by expired gases. Direct-acting vasodilators may be required for blood pressure control if the patient cannot tolerate the myocardial depressant effects of an inhaled anesthetic. Vasopressors and inotropic agents sometimes are required to support the circulation in response to anesthetic-induced vasodilation and cardiac depression. Utilizing 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, manipulations and cannulation of the aorta, rewarming during cardiopulmonary bypass, and sternal wiring. Intraoperative awareness from insufficient anesthesia may occur during cardiac surgery, especially if the anesthetist places a greater emphasis 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 9-4).


View this table:
[in this window]
[in a new window]
?
TABLE 9-4 Checklist for preparation to separate from cardiopulmonary bypass

?

?? ANESTHESIA IN THE IMMEDIATE POSTOPERATIVE PERIOD
 Top
 References
?
Continuous monitoring of physiological functions during transport to the postoperative intensive care unit is paramount because of the possibility of hemodynamic instability. Cardiac output, blood pressure, and vascular tone decrease acutely in the immediate postoperative period because surgical stimulation no longer increases sympathetic tone. Vasodilation also occurs from increases in cutaneous blood flow during active rewarming. Reducing positive pressure ventilatory support during weaning from mechanical ventilation may alter hemodynamic function by increasing venous return and decreasing pulmonary vascular resistance. Sedative-hypnotic or analgesic drugs administered in the immediate postoperative period contribute to changes in the circulatory state.

Anesthesia is required in the early postoperative period because of mechanical ventilatory support, hypothermia, and the possibility of hypertension and tachycardia from pain and tracheal intubation if abrupt emergence occurs. Several hours may be needed to achieve criteria for tracheal extubation (e.g., minimal bleeding, cardiovascular stability, systemic rewarming). 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, complete blood and platelet count, chemistry battery with blood urea nitrogen and serum creatinine, serum glucose, ECG, prothrombin time and partial thromboplastin time, and arterial blood gases.

Preemptive patient management during operation and in the early postoperative period can decrease intensive care unit and hospital length of stay after cardiac surgery.192 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 (e.g., 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.

Hemodynamic management of cardiac surgical patients is integrated with anesthetic management. The ability to rapidly establish a diagnosis and circulation during anesthesia is essential for safe conduct of cardiac operations. The challenge to maintain control of the cardiovascular system during the course of a typical operation is complicated by actions of the anesthetic drugs on the circulation, autonomic nervous system reflexes, variability in individual responses to vasoactive drug therapy, continuous fluctuations in the intensity of painful stimuli, rapid intravascular volume shifts, the patient's underlying medical condition, and the urgency of operation.


?? REFERENCES
 Top
?
  1. O'Connor MF, Daves SM, Tung A, et al: BIS monitoring to prevent awareness during general anesthesia. Anesthesiology 2001; 94:520.[Medline]
  2. Szekely B, Saint-Marc T, Degremont AC, et al: Value of bispectral index monitoring during cardiopulmonary resuscitation. Br J Anaesth 2002; 88:443.[Abstract/Free?Full?Text]
  3. Owens WD, Felts JA, Spitznagel EL: ASA Physical Status Classifications: a study of consistency of ratings. Anesthesiology 1978; 49:239.[Medline]
  4. Samsoon GLT, Young JRB: Difficult tracheal intubation: a retrospective study. Anaesthesia 1987; 42:487.[Medline]
  5. Mallampati SR, Gatt SP, Gugino LD, et al: A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J 1985; 32:429.[Medline]
  6. Strandgaard S, Olesen J, Skinhoj E, Lassen NA: Autoregulation of brain circulation in severe arterial hypertension. BMJ 1973; 1:507.
  7. Cheng EY, Lauer KK, Stommel KA, Guenther NR: Evaluation of the palmar circulation by pulse oximetry. J Clin Monit 1989; 5:1.[Medline]
  8. Bedford RF, Shah NK: Blood pressure monitoring: invasive and noninvasive, in Blitt CD, Hines RL (eds): Monitoring in Anesthesia and Critical Care Medicine, 3d ed. New York, Churchill Livingstone, 1995; p 95.
  9. O'Rourke MF: Pressure and flow waves in systemic arteries and the anatomical design of the arterial system. J Appl Physiol 1967; 23:139.[Free?Full?Text]
  10. Brunner JMR, Krenis LJ, Kunsman JM, et al: Comparison of direct and indirect methods of measuring arterial blood pressure, part I. Med Instrum 1981; 15:11.[Medline]
  11. Boutros A, Albert S: Effect of the dynamic response of transducer-tubing system on accuracy of direct blood pressure measurement in patients. Crit Care Med 1983; 11:124.[Medline]
  12. Prys-Roberts C: Measurement of intravascular pressure, in Saidman LJ, Smith NT (eds): Monitoring in Anesthesia. New York, Churchill Livingstone, 1978.
  13. London M, Hollenberg M, Wong M, et al: Intraoperative myocardial ischemia: localization by continuous 12-lead electrocardiography. Anesthesiology 1988; 69:232.[Medline]
  14. Mangano DT, Browner WS, Hollenberg M, et al: Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery. N Engl J Med 1990; 323:1781.[Abstract]
  15. Moller JT, Johannessen NW, Espersen K, et al: Randomized evaluation of pulse oximetry in 20,802 patients, II: perioperative events and postoperative complications. Anesthesiology 1993; 78:445.[Medline]
  16. Pan PH, Gravenstein N: Intraoperative pulse oximetry: frequency and distribution of discrepant data. J Clin Anesth 1994; 6:491.[Medline]
  17. Strazis KP, Fox AW: Malignant hyperthermia: a review of published cases. Anesth Analg 1993; 77:297.[Abstract]
  18. Murphy FL: Hazards of anesthesia, in Longnecker DE, Murphy FL (eds): Dripps Introduction to Anesthesia, 9th ed. Philadelphia, WB Saunders, 1996.
  19. Reed CR, Sessler CN, Glauser FL, Phelan BA: Central venous catheter infections: concepts and controversies. Intensive Care Med 1995; 21:177.[Medline]
  20. Troianos CA, Jobes DR, Ellison N: Ultrasound-guided cannulation of the internal jugular vein: a prospective, randomized study. Anesth Analg 1991; 72:823.[Medline]
  21. Van Daele ME, Sutherland GR, Mitchell MM, et al: Do changes in pulmonary capillary wedge pressure adequately reflect myocardial ischemia during anesthesia? A correlative preoperative hemodynamic, electrocardiographic and transesophageal echocardiographic study. Circulation 1990; 81:865.[Medline]
  22. Sprung CL, Elser B, Schein RMH, et al: Risk of right bundle branch block and complete heart block during pulmonary artery catheterization. Crit Care Med 1989; 17:1.[Medline]
  23. Kim YL, Richman KA, Marshall BE: Thrombocytopenia associated with Swan Ganz catheterization in patients. Anesthesiology 1980; 53:261.[Medline]
  24. Mangano DT: Heparin bonding and long-term protection against thrombogenesis. N Engl J Med 1982; 307:894.[Medline]
  25. Bohrer H, Fleischer F, Lang J, Vahl C: Early formation of thrombi on pulmonary artery catheters in cardiac surgical patients receiving high-dose aprotonin. J Cardiothorac Anesth 1990; 4:222.[Medline]
  26. Swan HJC, Ganz W, Forrester J, et al: Catheterization of the heart in man with use of a flow directed balloon tipped catheter. N Engl J Med 1970; 283:447.
  27. Reich DL, Kaplan JA: Hemodynamic monitoring, in Kaplan JA (ed): Cardiac Anesthesia. Philadelphia, WB Saunders, 1993; p 261.
  28. Savino JS, Troianos CA, Aukburg, et al: Measurement of pulmonary blood flow with transesophageal two-dimensional and Doppler echocardiography. Anesthesiology 1991; 75:445.[Medline]
  29. Philip JH, Feinstein DM, Raemer DB: Monitoring anesthetic and respiratory gases, in Blitt CD, Hines RL (eds): Monitoring in Anesthesia and Critical Care Medicine, 3d ed. New York, Churchill Livingstone, 1995; p 363.
  30. Cheung A, Chernow B: Perioperative electrolyte disorders, in Benumof JL, Saidman LJ (eds): Anesthesia and Perioperative Complications. St Louis, Mosby-Year Book, 1991; p 466.
  31. Drop LJ: Ionized calcium, the heart, and hemodynamic function. Anesth Analg 1985; 64:432.[Medline]
  32. Bronsky B, Dubin A, Waldstein SS, et al: Calcium and the electrocardiogram, 1: electrocardiographic manifestations of hypoparathyroidism. Am J Cardiol 1961; 7:823.
  33. Robertie PG, Butterworth JF, Royster RL, et al: Normal parathyroid hormone responses to hypocalcemia during cardiopulmonary bypass. Anesthesiology 1991; 75:43.[Medline]
  34. Fernandez-del Castillo C, Harringer W, Warshaw AL, et al: Risk factors for pancreatic cellular injury after cardiopulmonary bypass. N Engl J Med 1991; 325:382.[Abstract]
  35. Algio LS, Stanford GG, Maddi R, et al: Hypomagnesemia is common following cardiac surgery. J Cardiothorac Vasc Anesth 1991; 5:201.[Medline]
  36. England MR, Gordon G, Salem M, Chernow B: Magnesium administration and dysrhythmias after cardiac surgery: a placebo-controlled, double-blind, randomized trail. JAMA 1992; 268:2395[Abstract]
  37. Vyvyan HA, Mayne PN, Cutfield GR: Magnesium flux and cardiac surgery: a study of the relationship between magnesium exchange, serum magnesium levels and postoperative arrhythmias. Anaesthesia 1994; 49:245.[Medline]
  38. Furnary AP, Zerr KJ, Grunkemeier GL, Starr A: Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. Ann Thorac Surg 1999; 67:352.[Abstract/Free?Full?Text]
  39. van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in the surgical intensive care unit. N Eng J Med 2001; 345:1359[Abstract/Free?Full?Text]
  40. Floyd TF, Cheung AT, Stecker MM: Postoperative neurologic assessment and management of the cardiac surgical patient. Semin Thorac Cardiovasc Surg 2000; 12:337.[Medline]
  41. McKhann GM, Goldsborough MA, Borowicz LM Jr, et al: Predictors of stroke risk in coronary artery bypass patients. Ann Thorac Surg 1997; 63:516[Abstract/Free?Full?Text]
  42. Newman MF, Wolman R, Kanchuger M, et al: Multicenter preoperative stroke risk index for patients undergoing coronary artery bypass graft surgery. Multicenter Study of Perioperative Ischemia (McSPI) Research Group. Circulation 1996; 94:II74.
  43. Caplan LR, Hennerici M: Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol 1998; 55:1475.[Abstract/Free?Full?Text]
  44. van der Linden J, Hadjinikolaou L, Bergman P, Lindblom D: Postoperative stroke in cardiac surgery is related to the location and extent of atherosclerotic disease in the ascending aorta. J Am Coll Cardiol 2001; 38:131[Abstract/Free?Full?Text]
  45. Rokkas CK, Kouchoukos NT: Surgical management of the severely atherosclerotic ascending aorta during cardiac operations. Semin Thorac Cardiovasc Surg 1998; 10:240.[Medline]
  46. Dexter F, Hindman BJ: Effect of haemoglobin concentration on brain oxygenation in focal stroke: a mathematical modelling study. Br J Anaesth 1997; 79:346.[Abstract/Free?Full?Text]
  47. Goto T, Yoshitake A, Baba T, et al: Cerebral ischemic disorders and cerebral oxygen balance during cardiopulmonary bypass surgery: preoperative evaluation using magnetic resonance imaging and angiography. Anesth Analg 1997; 84:5.[Abstract]
  48. Chalela JA, Katzan I, Liebeskind DS, et al: Safety of intra-arterial thrombolysis in the postoperative period. Stroke 2001; 32:1365.[Abstract/Free?Full?Text]
  49. Moazami N, Smedira NG, McCarthy PM, et al: Safety and efficacy of intraarterial thrombolysis for perioperative stroke after cardiac operation. Ann Thorac Surg 2001; 72:1933.[Abstract/Free?Full?Text]
  50. Gravereaux EC, Faries PL, Burks JA, et al: Risk of spinal cord ischemia after endograft repair of thoracic aortic aneurysms. J Vasc Surg 2001; 34:997.[Medline]
  51. Coselli JS, LeMaire SA, Miller CC 3rd, et al: Mortality and paraplegia after thoracoabdominal aortic aneurysm repair: a risk factor analysis. Ann Thorac Surg 2000; 69:409.[Abstract/Free?Full?Text]
  52. Safi HJ, Miller CC 3rd: Spinal cord protection in descending thoracic and thoracoabdominal aortic repair. Ann Thorac Surg 1999; 67:1937.[Abstract/Free?Full?Text]
  53. Grabitz K, Sandmann W, Stuhmeier K, et al: The risk of ischemic spinal cord injury in patients undergoing graft replacement for thoracoabdominal aortic aneurysms. J Vasc Surg 1996; 23:230.[Medline]
  54. Griepp RB, Ergin MA, Galla JD, et al: Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta. J Thorac Cardiovasc Surg 1996; 112:1202.[Abstract/Free?Full?Text]
  55. Svensson LG, Hess KR, Coselli JS, Safi HJ: Influence of segmental arteries, extent, and atriofemoral bypass on postoperative paraplegia after thoracoabdominal aortic operations. J Vasc Surg 1994; 20:255.[Medline]
  56. van Dongen EP, Schepens MA, Morshuis WJ, et al: Thoracic and thoracoabdominal aortic aneurysm repair: use of evoked potential monitoring in 118 patients. J Vasc Surg 2001; 34:1035.[Medline]
  57. Jacobs M, Meylaerts SA, de Haan P, et al: Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair. J Vasc Surg 1999; 29:48.[Medline]
  58. Shiiya N, Yasuda K, Matsui Y, et al: Spinal cord protection during thoracoabdominal aortic aneurysm repair: results of selective reconstruction of the critical segmental arteries guided by evoked spinal cord potential monitoring. J Vasc Surg 1995; 21:970.[Medline]
  59. Svensson LG: Management of segmental intercostal and lumbar arteries during descending and thoracoabdominal aneurysm repairs. Semin Thorac Cardiovasc Surg 1998; 10:45.[Medline]
  60. Ross SD, Kron IL, Parrino PE, et al: Preservation of intercostal arteries during thoracoabdominal aortic aneurysm surgery: a retrospective study. J Thorac Cardiovasc Surg 1999; 118:17.[Abstract/Free?Full?Text]
  61. Albin MS, White RJ, Locke GE, Kretchmer HE: Spinal cord hypothermia by localized perfusion cooling. Nature 1966; 210:1059.[Medline]
  62. Cambria RP, Davison JK: Regional hypothermia for prevention of spinal cord ischemic complications after thoracoabdominal aortic surgery: experience with epidural cooling. Semin Thorac Cardiovasc Surg 1998; 10:61.[Medline]
  63. Bonatti J, Watzka S, Antretter H, et al: Spinal cord protection in descending and thoracoabdominal aortic surgerythe role of distal perfusion. Thorac Cardiovasc Surg 1996; 44:136.[Medline]
  64. Robertazzi RR, Acinapura AJ: The efficacy of left atrial to femoral artery bypass in the prevention of spinal cord ischemia during aortic surgery. Semin Thorac Cardiovasc Surg 1998; 10:67.[Medline]
  65. Ling E, Arellano R: Systematic overview of the evidence supporting the use of cerebrospinal fluid drainage in thoracoabdominal aneurysm surgery for prevention of paraplegia. Anesthesiology 2000; 93:1115.[Medline]
  66. Azizzadeh A, Huynh TT, Miller CC 3rd, Safi HJ: Reversal of twice-delayed neurologic deficits with cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a national database collection. J Vasc Surg 2000; 31:592.[Medline]
  67. Ortiz-Gomez JR, Gonzalez-Solis FJ, Fernandez-Alonso L, Bilbao JI: Reversal of acute paraplegia with cerebrospinal fluid drainage after endovascular thoracic aortic aneurysm repair. Anesthesiology 2001; 95:1288.[Medline]
  68. Weaver KD, Wiseman DB, Farber M, et al: Complications of lumbar drainage after thoracoabdominal aortic aneurysm repair. J Vasc Surg 2001; 34:623.[Medline]
  69. Newman MF, et al: Longitudinal assessment of neurocognitive function after coronary-artery bypass surgery. N Engl J Med 2001; 344:395.[Abstract/Free?Full?Text]
  70. Vingerhoets G, Van Nooten G, Vermassen F, et al: Short-term and long-term neuropsychological consequences of cardiac surgery with extracorporeal circulation. Eur J Cardiothorac Surg 1997; 11:424.[Abstract]
  71. Selnes OA, Goldsborough MA, Borowicz LM Jr, et al: Determinants of cognitive change after coronary artery bypass surgery: a multifactorial problem. Ann Thorac Surg 1999; 67:1669.[Abstract/Free?Full?Text]
  72. Mutch WA, Sutton IR, Teskey JM, et al: Cerebral pressure-flow relationship during cardiopulmonary bypass in the dog at normothermia and moderate hypothermia. J Cereb Blood Flow Metab 1994; 14:510.[Medline]
  73. Braekken SK, Russell D, Brucher R, et al: Cerebral microembolic signals during cardiopulmonary bypass surgery: frequency, time of occurrence, and association with patient and surgical characteristics. Stroke 1997; 28:1988.[Abstract/Free?Full?Text]
  74. Heyer EJ, Delphin E, Adams DC, et al: Cerebral dysfunction after cardiac operations in elderly patients. Ann Thorac Surg 1995; 60:1716.[Abstract/Free?Full?Text]
  75. Jonas RA: Optimal hematocrit for adult cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2001; 15:672.
  76. Harris DN, Oatridge A, Dob D, et al: Cerebral swelling after normothermic cardiopulmonary bypass. Anesthesiology 1998; 88:340.[Medline]
  77. Grigore AM, Grocott HP, Mathew JP, et al: The rewarming rate and increased peak temperature alter neurocognitive outcome after cardiac surgery. Anesth Analg 2002; 94:4.[Abstract/Free?Full?Text]
  78. Cook DJ, Oliver WC Jr, Orszulak TA, Daly RC: A prospective, randomized comparison of cerebral venous oxygen saturation during normothermic and hypothermic cardiopulmonary bypass. J Thorac Cardiovasc Surg 1994; 107:1020.[Abstract/Free?Full?Text]
  79. Patel RL, Turtle MR, Chambers DJ, et al: Alpha-stat acid-base regulation during cardiopulmonary bypass improves neuropsychologic outcome in patients undergoing coronary artery bypass grafting. J Thorac Cardiovasc Surg 1996; 111:1267.[Abstract/Free?Full?Text]
  80. Undar A, Calhoon JH, Cossman RM, Johnson SB: The effects of pulsatile cardiopulmonary bypass on cerebral and renal blood flow in dogs [letter; comment]. J Cardiothorac Vasc Anesth 1998; 12:126.[Medline]
  81. Croughwell ND, Reves JG, White WD, et al: Cardiopulmonary bypass time does not affect cerebral blood flow. Ann Thorac Surg 1998; 65:1226.[Abstract/Free?Full?Text]
  82. Sungurtekin H, Plochl W, Cook DJ: Relationship between cardiopulmonary bypass flow rate and cerebral embolization in dogs. Anesthesiology 1999; 91:1387.[Medline]
  83. Jacobs A, Neveling M, Horst M, et al: Alterations of neuropsychological function and cerebral glucose metabolism after cardiac surgery are not related only to intraoperative microembolic events. Stroke 1998; 29:660.[Abstract/Free?Full?Text]
  84. Tardiff BE, Newman MF, Saunders AM, et al: Preliminary report of a genetic basis for cognitive decline after cardiac operations. The Neurologic Outcome Research Group of the Duke Heart Center. Ann Thorac Surg 1997; 64:715.[Abstract/Free?Full?Text]
  85. Boyle EM Jr, Pohlman TH, Johnson MC, Verrier ED: Endothelial cell injury in cardiovascular surgery: the systemic inflammatory response. Ann Thorac Surg 1997; 63:277.[Abstract/Free?Full?Text]
  86. Zuccala G, Onder G, Pedone C, et al: Cognitive dysfunction as a major determinant of disability in patients with heart failure: results from a multicentre survey. On behalf of the GIFA (SIGG-ONLUS) Investigators. J Neurol Neurosurg Psychiatry 2001; 70:109.[Abstract/Free?Full?Text]
  87. Almeida OP, Flicker L: The mind of a failing heart: a systematic review of the association between congestive heart failure and cognitive functioning. Intern Med J 2001; 31:290.[Medline]
  88. Stanimirovic D, Satoh K: Inflammatory mediators of cerebral endothelium: a role in ischemic brain inflammation. Brain Pathol 2000; 10:113.[Medline]
  89. Starzyk RM, Rosenow C, Frye J, et al: Cerebral cell adhesion molecule: a novel leukocyte adhesion determinant on blood-brain barrier capillary endothelium. J Infect Dis 2000; 181:181.[Medline]
  90. Abbott NJ: Inflammatory mediators and modulation of blood-brain barrier permeability. Cell Mol Neurobiol 2000; 20:131.[Medline]
  91. Riis J, Lomholt B, Haxholdt O, et al: Immediate and long-term mental recovery from general versus epidural anesthesia in elderly patients. Acta Anaesthesiol Scand 1983; 27:44.[Medline]
  92. Turnipseed WD, Berkoff HA, Belzer FO: Postoperative stroke in cardiac and peripheral vascular disease. Ann Surg 1980; 192:365.[Medline]
  93. Bedford PD: Adverse cerebral effects of anaesthesia in old people. Lancet 1955; 2:259.
  94. Moller JT, Cluitmans P, Rasmussen LS, et al: Long-term postoperative cognitive dysfunction in the elderly ISPOCD1 study. ISPOCD investigators. International Study of Post-Operative Cognitive Dysfunction [see comments] [published erratum appears in Lancet 1998; 351:1742]. Lancet 1998; 351:857.[Medline]
  95. Abildstrom H, Rasmussen LS, Rentowl P, et al: Cognitive dysfunction 12 years after non-cardiac surgery in the elderly. ISPOCD group. International Study of Post-Operative Cognitive Dysfunction. Acta Anaesthesiol Scand 2000; 44:1246.[Medline]
  96. Kofke WA, Garman RH, Garman R, Rose ME et al: Opioid neurotoxicity: fentanyl-induced exacerbation of cerebral ischemia in rats. Brain Res 1999; 818:326.[Medline]
  97. Personnet F, Sindon M, Laviron A, et al: Human cortical electrogenesis: stratigraphy and spectral analysis, in Petsche H, Brazier MAB (eds): Synchronization of EEG Activity in Epilepsies. New York, Springer-Verlag, 1972; p 235.
  98. Allison T: Calculated and empirical evoked-potential distribution in human recordings, in Otto DA (ed): Multidisciplinary Perspectives in Event-Related Brain Potential Research. Washington, DC, US Environmental Protection Agency, 1978.
  99. Bashein G, Nessly ML, Bledsoe SW, et al: Electroencephalography during surgery with cardiopulmonary bypass and hypothermia. Anesthesiology 1992; 76:878.[Medline]
  100. Levy WJ: Monitoring of the electroencephalogram during cardiopulmonary bypass. Anesthesiology 1992; 76:876.[Medline]
  101. Markand ON, Warren C, Mallik GS, et al: Temperature-dependent hysteresis in somatosensory and auditory evoked potentials. Electroencephalogr Clin Neurophysiol 1990; 77:425.[Medline]
  102. Cheung AT, Savino JS, Weiss SJ, et al: Detection of acute embolic stroke during mitral valve replacement using somatosensory evoked potential monitoring. Anesthesiology 1995; 83:208.[Medline]
  103. Hickey C, Gugino LD, Aglio LS: Intraoperative somatosensory evoked potential monitoring predicts peripheral nerve injury during cardiac surgery. Anesthesiology 1993; 78:29.[Medline]
  104. Clark RE, Brillman J, Davis DA, et al: Microemboli during coronary artery bypass grafting. J Thorac Cardiovasc Surg 1995; 109:249.[Abstract/Free?Full?Text]
  105. Cheung AT, Weiss SJ, Savino JS: Protamine-induced right-to-left intracardiac shunting. Anesthesiology 1991; 75:904.[Medline]
  106. Weiss SJ, Cheung AT, Stecker MM, et al: Fatal paradoxical cerebral embolization during bilateral knee arthroplasty. Anesthesiology 1996; 84:721.[Medline]
  107. Pearson AC, Labovitz AJ, Tatineni S, Gomez CR: Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology. J Am Coll Cardiol 1991; 17:66.[Abstract]
  108. Cheung AT, Levin SK, Weiss SJ, et al: Intracardiac thrombus: a risk of incomplete anticoagulation for cardiac operations. Ann Thorac Surg 1994; 58:541.[Abstract]
  109. Savino JS, Weiss SJ: Images in clinical medicine: right atrial tumor. N Engl J Med 1995; 333:1608.[Free?Full?Text]
  110. Davila-Roman VG, Barzilai B, Wareing TH, et al: Intraoperative ultrasonographic evaluation of the ascending aorta in 100 consecutive patients undergoing cardiac surgery. Circulation 1991; 84(suppl III):III47.
  111. Tuman KJ, McCarthy RJ, Spiess BD, Ivankovich AD: Comparison of anesthetic techniques in patients undergoing heart valve replacement. J Cardiothorac Anesth 1990; 4:159.[Medline]
  112. Tuman KJ, McCarthy RJ, Spiess BD, et al: Does choice of anesthetic agent significantly affect outcome after coronary artery surgery? Anesthesiology 1989; 70:189.[Medline]
  113. Slogoff S, Keats AS: Randomized trial of primary anesthetic agents on outcome of coronary artery bypass operations. Anesthesiology 1989; 70:179.[Medline]
  114. Mora CT, Dudek C, Torjman MC, White PF: The effects of anesthetic technique on the hemodynamic response and recovery profile in coronary revascularization patients. Anesth Analg 1995; 81:900.[Abstract]
  115. James KB, Marwick T, Cosgrove DML: Underestimation of mitral regurgitation under general anesthesia. J Thorac Cardiovasc Surg 1992; 104:534.[Medline]
  116. Konstadt SN, Louie EK, Shore-Lesserson L, et al: The effects of loading changes on intraoperative Doppler assessment of mitral regurgitation. J Cardiothorac Vasc Anesth 1994; 8:19.
  117. Longnecker DE, Cheung AT: Pharmacology of inhalational anesthetics, in Longnecker DE, Tinker JH, Morgan GE (eds): Principles and Practice of Anesthesiology, 2d ed. St Louis, Mosby, 1998; p 1123.
  118. Kikura M, Ikeda K: Comparison of effects of sevoflurane/nitrous oxide and enflurane/nitrous oxide on myocardial contractility in humans. Anesthesiology 1992; 79:235.
  119. Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog. Anesthesiology 1991; 74:539.[Medline]
  120. Stowe DF, Monroe SM, Marijic J, et al: Comparison of halothane, enflurane, and isoflurane with nitrous oxide on contractility and oxygen supply and demand in isolated hearts. Anesthesiology 1991; 75:1062.[Medline]
  121. Kemmotsu S, Hasimoto Y, Sheimosato S: Inotropic effects of isoflurane on mechanics of contraction in isolated cat papillary muscles from normal and failing hearts. Anesthesiology 1973; 39:470.[Medline]
  122. Brown BR, Richard J: A comparative study of the effects of five general anesthetics on myocardial contractility: isometric conditions. Anesthesiology 1971; 34:236.[Medline]
  123. Van Tright P, Christian CC, Fagraeus L, et al: Myocardial depression by anesthetic agents: quantitation based on end-systolic pressure-dimension relations. Am J Cardiol 1984; 53:243.[Medline]
  124. Kotrly KJ, Ebert TH, Vucins E, et al: Baroreflex reflex control of heart rate during isoflurane anesthesia in humans. Anesthesiology 1984; 60:173.[Medline]
  125. Pagel PS, Kampine JP, Schmeling WT, Warltier DC: Alteration of left ventricular diastolic function by desflurane, isoflurane, and halothane in the chronically instrumented dog with autonomic nervous system blockade. Anesthesiology 1991; 74:1103.[Medline]
  126. Buffington CW: Impaired systolic thickening associated with halothane in the presence of a coronary stenosis is mediated by changes in hemodynamics. Anesthesiology 1986; 64:632.[Medline]
  127. Gelman S, Fowler KC, Smith LR: Regional blood flow during isoflurane and halothane anesthesia. Anesth Analg 1984; 63:557.[Abstract]
  128. Blaise G, Sill JC, Nugent M, et al: Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries. Anesthesiology 1987; 67:513.[Medline]
  129. Becker LC: Conditions for vasodilator-induced coronary steal in experimental myocardial ischemia. Circulation 1978; 57:1103.[Medline]
  130. Hogue CW Jr, Lerbst TJ, Pond C, et al: Perioperative myocardial ischemia. Anesthesiology 1993; 79:514.[Medline]
  131. Helman JD, Leung JM, Bellows WH, et al: The risk of myocardial ischemia in patients receiving desflurane versus sufentanil anesthesia for coronary artery bypass graft surgery. Anesthesiology 1992; 77:47.[Medline]
  132. Inoue K, Reichelt W, el-Banayosy A, et al: Does isoflurane lead to a higher incidence of myocardial infarction and perioperative death than enflurane in coronary artery surgery? A clinical study of 1178 patients. Anesth Analg 1990; 71:469.[Abstract]
  133. Ebert TJ, Muzi M: Sympathetic hyperactivity during desflurane anesthesia in healthy volunteers. Anesthesiology 1993; 79:444.[Medline]
  134. Zaugg M, Lucchinetti E, Spahn D, Pasch T, Schaub M: Volatile anesthetics mimic cardiac preconditioning by priming the activation of mito KATP channels via multiple signaling pathways. Anesthesiology 2002: 97:4.[Medline]
  135. Zaugg M, Lucchinetti E, Spahn D, et al: Differential effects of anesthetics on mitochondrial KATP channel activity and cardiomyocyte protection. Anesthesiology 2002; 97:15.[Medline]
  136. Siemikawa K, Ishizseka N, Suzaki M: Arrhythmogenic plasma levels of epinephrine with halothane, enflurane, and pentobarbital anesthesia in the dog. Anesthesiology 1983; 58:322.[Medline]
  137. Thomson IR, Bowering JB, Hudson RJ, et al: A comparison of desflurane and isoflurane in patients undergoing coronary artery surgery. Anesthesiology 1991; 75:776.[Medline]
  138. Cheung AT, Marshall BE: The inhaled anesthetics, in Longnecker DE, Murphy FL (eds): Dripps Introduction to Anesthesia, 9th ed. Philadelphia, WB Saunders, 1996.
  139. Varadarajan SG, An J, Novalija E, Stowe DF. Sevoflurane before or after ischemia improves contractile and metabolic function while reducing myoplasmic Ca(2+) loading in intact hearts. Anesthesiology 2002; 96:125.[Medline]
  140. Loeckinger A, Keller C, Lindner KH, Kleinsasser A: Pulmonary gas exchange in coronary artery surgery patients during sevoflurane and isoflurane anesthesia. Anesth Analg 2002; 94:1107.[Abstract/Free?Full?Text]
  141. Stowe DF, Bosnjak ZJ, Kampine JP: Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts. Anesth Analg 1992; 74:547.[Abstract]
  142. Park WK, Lynch C III: Propofol and thiopental depression of myocardial contractility: a comparative study of mechanical and electrophysiologic effects in isolated guinea pig ventricular muscle. Anesth Analg 1992; 74:395.[Abstract]
  143. Lepage J-YM, Pinaud ML, Helias JH, et al: Left ventricular performance during propofol and methohexital anesthesia: isotopic and invasive cardiac monitoring. Anesth Analg 1991; 73:3.[Abstract]
  144. Muzi M, Berens RA, Kampine JP, Ebert TJ: Ventilation contributes to propofol-mediated hypotension in humans. Anesth Analg 1992; 74:877.[Abstract]
  145. Rouby JJ, Andreev A, Leger P, et al: Peripheral vascular effects of thiopental and propofol in humans with artificial hearts. Anesthesiology 1991; 75:32.[Medline]
  146. Gooding JM, Corssen G: Effect of etomidate on the cardiovascular system. Anesth Analg 1977; 56:717.[Abstract]
  147. Riou B, Lecarpentier Y, Chemla D, Viars P: In vitro effects of etomidate on intrinsic myocardial contractility in the rat. Anesthesiology 1990; 72:330.[Medline]
  148. Riou B, Lecarpentier Y, Viars P: Effects of etomidate on the cardiac papillary muscle of normal hamsters and those with cardiomyopathy. Anesthesiology 1993; 78:83.[Medline]
  149. White PF, Way WL, Trevor AJ: Ketamine-Mits pharmacology and therapeutic uses. Anesthesiology 1982; 56:119.[Medline]
  150. Waxman K, Shoemaker WC, Lippmann M: Cardiovascular effects of anesthetic induction with ketamine. Anesth Analg 1980; 59:355.[Abstract]
  151. Flacke JW, Bloor BC, Flacke WE, et al: Reduced narcotic requirement by clonidine with improved hemodynamic and adrenergic stability in patients undergoing coronary bypass surgery. Anesthesiology 1987; 67:11.[Medline]
  152. Schulz R, Guth BD, Heusch G: Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia. Cardiovasc Drugs Ther 1989; 3:L43.
  153. Talke P, Li J, Jjain U, et al: Effects of perioperative dexmedetomidine infusion in patients undergoing vascular surgery: the study of perioperative ischemia research group. Anesthesiology 1995; 82:620.[Medline]
  154. Mansour A., Khachaturian H, Lewis ME, et al: Anatomy of CNS opioid receptors. Trends Neurosci 1988; 11:308.[Medline]
  155. Bovill JG, Boer F: Opioids in cardiac anesthesia, in Kaplan J (ed): Cardiac Anesthesia, 3d ed. Philadelphia, WB Saunders, 1993; p 467.
  156. Benthuysen JL, Smith NT, Sanford TJ, et al: Physiology of alfentanil-induced rigidity. Anesthesiology 1986; 64:440.[Medline]
  157. Smith NT, Benthuysen JL, Bickford RG, et al: Seizures during opioid anesthetic induction: are they opioid induced rigidity? Anesthesiology 1989; 71:852.[Medline]
  158. Azar I, Turndorf H: Severe hypertension and multiple atrial premature contractions following naloxone administration. Anesth Analg 1979; 58:524.[Medline]
  159. Gal TJ, DiFazio CA: Prolonged antagonism of opioid action with intravenous nalmefene in man. Anesthesiology 1986; 64:175.[Medline]
  160. Bailey PL, Clark NJ, Pace NL, et al: Failure of nalbuphine to antagonize morphine: a double-blind comparison with naloxone. Anesth Analg 1986; 65:605.[Abstract]
  161. Puttfarcken PS, Cox BM: Morphine induced desensitizations and down-regulation at mu receptors in 7315c pituitary tumor cells. Life Sci 1989; 45:1937.[Medline]
  162. Shafer A, White PF, Schuttlrt J, Rosenthal MH: Use of fentanyl infusion in the intensive care unit: tolerance to its anesthetic effects? Anesthesiology 1983; 59:245.[Medline]
  163. Egan TD, Lemmens HJ, Fiset P, et al: The pharmacokinetics of the new short-acting opioid remifentanil (GI87084B) in healthy adult male volunteers. Anesthesiology 1993; 79:881.[Medline]
  164. Douglas JA, Tuxen DV, Horne M, et al: Myopathy in severe asthma. Am Rev Respir Dis 1992; 146:517.[Medline]
  165. Backman SB, Stein RD, Ralley FE, Fox GS: Neostigmine-induced bradycardia following recent vs remote cardiac transplantation in the same patient. Can J Anaesth 1996; 43(4):394.[Abstract/Free?Full?Text]
  166. Santos AC, DeArmas PI: Systemic toxicity of levobupivacaine, bupivacaine, and ropivacaine during continuous intravenous infusion to nonpregnant and pregnant ewes. Anesthesiology 2001; 95:1256.[Medline]
  167. Ohmura S, Kawada M, Ohta T, et al: Systemic toxicity and resuscitation in bupivacaine-, levobupivacaine-, or ropivacaine-infused rats. Anesth Analg 2001; 93:743.[Abstract/Free?Full?Text]
  168. American Society of Anesthesiologists Task Force on Management of the Difficult Airway: Practice guidelines for management of the difficult airway. Anesthesiology 1993; 78:597.[Medline]
  169. Swenson JD, Hullander RM, Wingler K, Leivers D: Early extubation after cardiac surgery using combined intrathecal sufentanil and morphine. J Cardiothorac Vasc Anesth 1994; 8:509.[Medline]
  170. Fitzpatrick GJ, Moriarty DC: Intrathecal morphine in the management of pain following cardiac surgery: a comparison with morphine IV. Br J Anaesth 1988; 60:639.[Abstract/Free?Full?Text]
  171. Aun C, Thomas D, St. John-Jones L, et al: Intrathecal morphine in cardiac surgery. Eur J Anaesth 1985; 2:419.[Medline]
  172. Scott NB, Turfrey DJ, Ray AA, et al: A prospective randomized study of the potential benefits of thoracic epidural anesthesia and analgesia in patients undergoing coronary artery bypass grafting. Anesth Analg 2001; 93:528.[Abstract/Free?Full?Text]
  173. Moore R, Follette DM, Berkoff HA: Poststernotomy fractures and pain management in open cardiac surgery. Chest 1994; 106:1339.[Abstract/Free?Full?Text]
  174. Robinson RJ, Brister S, Jones E, Quigly M: Epidural meperidine analgesia after cardiac surgery. Can Anaesth Soc J 1986; 33:550.[Medline]
  175. Vandermeulen EP, Van Aken H, Vermylen J: Anticoagulants and spinal-epidural anesthesia. Anesth Analg 1994; 79:1165.[Medline]
  176. Blomberg S, Curelaru I, Emanuelsson H, et al: Thoracic epidural anaesthesia in patients with unstable angina pectoris. Eur Heart J 1989; 10:437.[Abstract/Free?Full?Text]
  177. Blomberg SG: Long-term home self-treatment with high thoracic epidural anesthesia in patients with severe coronary artery disease. Anesth Analg 1994; 79:413.[Abstract]
  178. Goertz AW, Seeling W, Heinrich H, et al: Influence of high thoracic epidural anesthesia on left ventricular contractility assessed using the end-systolic pressure-length relationship. Acta Anaesthesiol Scand 1993; 37:38.[Medline]
  179. Blomberg S, Curelaru I, Emanuelsson H, et al: Thoracic epidural anaesthesia in patients with unstable angina pectoris. Eur Heart J 1989; 10:437.
  180. Reiz S, Nath S, Rais O: Effects of thoracic epidural block and prenalterol on coronary vascular resistance and myocardial metabolism in patients with coronary artery disease. Acta Anaesthesiol Scand 1980; 24:11.[Medline]
  181. Blomberg S, Emanuelsson H, Ricksten SE: Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris. Anesth Analg 1989; 65:558.
  182. Kock M, Blomberg S, Emanuelsson H, et al: Thoracic epidural anesthesia improves global and regional left ventricular function during stress-induced myocardial ischemia in patients with coronary artery disease. Anesth Analg 1990; 71:625.[Abstract]
  183. Acher CW, Wynn MM, Archibald J: Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms. Surgery 1990; 108:755.[Medline]
  184. Blaisdell FW, Cooley DA: The mechanism of paraplegia after temporary thoracic aortic occlusion and its relationship to spinal fluid pressure. Surgery 1962; 51:1351.
  185. Svensson MB, Von Ritter CM, Groeneveld HT, et al: Cross-clamping of the thoracic aorta: influence of aortic shunts, laminectomy, papaverine, calcium channel blocker, allopurinol and superoxide dismutase on spinal cord blood flow and paraplegia in baboons. Ann Surg 1986; 204:388.
  186. Bower TC, Murray MJ, Gloviczki P, et al: Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome. J Vasc Surg 1988; 9:135.
  187. Murray MJ, Werner E, Oliver WC, et al: Anesthetic management of descending thoracic and thoracoabdominal aortic aneurysm repair: effects of CSF drainage and mild hypothermia. J Cardiothorac Vasc Anesth 1993; 7:266.[Medline]
  188. Crawford ES, Svensson LG, Hess KR, et al: A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high risk surgery on the thoracoabdominal aorta. J Vasc Surg 1991; 13:36.[Medline]
  189. Cheung AT, Weiss SJ, McGarvey M, et al: Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction. Ann Thorac Surg 2002; 74:413.[Abstract/Free?Full?Text]
  190. ACC/AHA guidelines and indications for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on cardiovascular procedures. Circulation 1991; 83:1125.[Medline]
  191. Practice guidelines for pulmonary artery catheterization: a report by the American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Anesthesiology 1993; 78:380.[Medline]
  192. Ramsay JG, DeLima LGR, Wynands JE, et al: Pure opioid vs opioid-volatile anesthesia for coronary artery bypass graft surgery: a prospective randomized double-blinded study. Anesth Analg 1994; 78:867.[Abstract]




This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this book
Right arrow Author home page(s):
Albert T. Cheung
Google Scholar
Right arrow Articles by Savino, J. S.
Right arrow Articles by Cheung, A. T.
Right arrow Articles citing this Article
Right arrow Search for Related Content
PubMed
Right arrow Articles by Savino, J. S.
Right arrow Articles by Cheung, A. T.
Related Collections
Right arrow Anesthesia