1 Intraoperative 1 Hemodynamic...

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Intraoperative Hemodynamic

MonitoringRebecca A. Schroeder, Shahar Bar-Yosef, and

Jonathan B. Mark

Key Points

• The combination of V5 with another lead (II, III, V4, or V6) increases the sensitivity of ischemia detection to 90%.

• In high-risk patients, most intraoperative ST segment changes occur in the absence of major hemodynamic lability, and maintenance of hemodynamic variables (blood pressure and heart rate) to within 20% of baseline values does not appear to reduce intraoperative ischemic events.

• Electrocardiograph (ECG) monitoring for myocardial ischemia augmented by continuous, computerized ECG monitors should be continued into the early postopera-tive period for high-risk patients.

• Invasive blood pressure monitoring is indicated when (1) large or abrupt hemodynamic changes are anticipated intraoperatively, (2) coexisting disease necessitates close hemodynamic management, (3) pharmacologic or mechanical intervention is anticipated or planned, or (4) noninvasive methods are impractical or impossible.

• Excessive variation of the systolic blood pressure (>15 mm Hg) is a strong predictor of occult hypovolemia.

• Overall, the risk of an ischemic complication from peripheral arterial catheterization is less than 0.1%.

• Central venous pressure (CVP) refl ects the balance among intravascular volume, venous tone, and right ventricular function.

• In general, a single isolated CVP value provides little information unless it is very high or very low.

• Recent development of small, portable ultrasound machines has made it possible to image the great veins of the neck prior to or during placement of central venous catheters. This has been shown in multiple clinical

studies as well as in a recent meta-analysis to decrease the incidence of failed catheter placement as well as the complication rate, especially in high-risk patients.

• Pulmonary artery catheter (PAC)-derived fi lling pres-sures are a poor index of right and left ventricular preload as they are infl uenced by heart rate, valvular disease, myocardial compliance, myocardial ischemia, and posi-tive pressure ventilation.

• Perioperative goal-directed therapy, that is, the “optimi-zation” of oxygen delivery and cardiac index, has been shown to reduce mortality, complications, and hospital length of stay in high-risk surgical patients.

• According to current American Society of Anesthesiolo-gists (ASA) recommendations, the use of PAC is consid-ered necessary only in high-risk patients undergoing high-risk surgery, and under the condition that the practice environment is favorable (i.e., knowledgeable and experienced physicians and intensive care unit nurses).

• Mixed venous oxygen saturation depends on the balance between oxygen delivery and consumption, and might be one of the more telling indices for judging the adequacy of the patient’s hemodynamic status.

• Thermodilution is the standard method for measuring cardiac output; it is subject, however, to intrinsic vari-ability, effect of intracardiac shunts and right-sided val-vular regurgitation, and infl uence of other factors affecting instantaneous blood temperature.

• Two newer cardiac output measurement methods that obviate the need for a PAC include the transpulmonary arterial thermodilution and the lithium dilution. Both seem to offer accuracy similar to the traditional thermo-dilution method.

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Cardiovascular Changes During Anesthesia and Positive Pressure Ventilation. . . . . . . . . . . . . . . 2516

Electrocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2517Arterial Blood Pressure Monitoring. . . . . . . . . . . . . . . . 2519Central Venous Pressure Monitoring. . . . . . . . . . . . . . . 2522

Pulmonary Artery Catheterization . . . . . . . . . . . . . . . . 2524Cardiac Output Monitoring . . . . . . . . . . . . . . . . . . . . . . 2531Intraoperative Transesophageal Echocardiography. . . . 2534Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2539

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• Several methods exist for continuous measurement of cardiac output. The fi rst method employs a modifi ed PAC with a blood-warming fi lament. It does not produce true real-time continuous measurements, but rather a trend of recent measurements over a couple of minutes.

• Esophageal Doppler cardiac output (CO) measurement employs a probe inserted into the lower esophagus to measure descending aorta blood fl ow. It tends to under-estimate CO measured by other methods, although accu-rately tracking changes occurring over time.

• Pulse contour methods derive continuous beat-to-beat CO from the arterial pressure waveform. In ventilated patients, they also allow measurement of stroke volume variation, an index of the adequacy of cardiac preload.

• Despite its classifi cation as category II for use in routine coronary artery bypass graft (CABG) surgery, transesoph-ageal echocardiography (TEE) in high-risk patients seems to be associated with better outcome.

• Transesophageal echocardiography has become invalu-able in planning for mitral valve repair and reconstruc-tion with excellent agreement between mechanism and location between TEE and surgical fi ndings.

• Following valve repair or replacement, TEE is especially useful in immediate evaluation of paravalvular leaks, leafl et motion, and other forms of valvular dysfunction.

• Although TEE has been reported to be more predictive than ECG in identifying patients who suffer periopera-tive myocardial infarction, concordance between TEE and ECG-detected ischemia is poor.

• Direct complications of TEE are the result of mechanical trauma to the upper gastrointestinal tract and orophar-ynx, and include abrasion, laceration, and perforation.

As with the practice of medicine that uses history taking and physical examination, effective use of cardiovascular moni-toring techniques requires technical skills, an understand-ing of function of these monitors, and the ways in which pathophysiologic states may be identifi ed and quantifi ed using these devices. In the perioperative setting, use of anesthetic drugs, positive pressure ventilation, and surgical interventions all cause signifi cant cardiovascular changes. Detection of these changes before irreversible harm ensues is the goal of hemodynamic monitoring. Thus, a hierarchy of monitoring methods has developed, dictated by individual circumstances. Invasive monitoring places the patient at risk from associated complications, and in each case, the poten-tial benefi ts must be weighed against these risks. For example, during general anesthesia, detection of myocardial ischemia using ST-segment electrocardiography (ECG) monitoring is clearly superior to clinical examination and is recommended for all patients with risk factors for coronary artery disease. In contrast, pulmonary artery catheter (PAC) monitoring should be reserved for a subset of those patients who have severe cardiovascular disease or who are undergoing exten-sive surgical procedures.

Historically, anesthesiologists relied heavily on clinical assessment of ventilation pattern, pupil size, muscle tone, skin color and pulse character. Electronic monitors allow physiologic variables not accessible by physical assessment to be measured accurately, and to be displayed and recorded at frequent intervals or even continuously. Monitors are

designed to augment rather than replace clinical skills and thereby improve clinical judgment and diagnosis. Automated devices incorporating alarms and data recorders free the cli-nician from laborious clerical tasks that detract from patient care. Powerful microprocessors have allowed miniaturiza-tion of bedside recording devices that can connect to hospital networks for printing of records and downloading of data. The creation of standardized anesthesia-related databases allows analysis and comparison of stored information within and between institutions for the purposes of audit and clinical research.

The clinical anesthesiologist provides a vital role in car-diovascular monitoring through careful observation and integration of monitored information and sound judgment based on experience and knowledge of individual patient circumstances. Of equal importance, however, when sophis-ticated monitoring systems fail, the physician must have the responsible medical skills to provide the critical safety net for patients undergoing surgical procedures.

Cardiovascular Changes During Anesthesia and Positive Pressure Ventilation

Induction of general anesthesia attenuates many compensa-tory cardiovascular refl exes, and almost all drugs used to induce general anesthesia are cardiovascular depressants (Table 119.1). As a result, it is normal for blood pressure and cardiac output to fall following induction of anesthesia. Most anesthetics produce dose-dependent cardiovascular changes. In any individual patient, both preoperative disease and hemodynamic state infl uence these changes. Signifi cantly exaggerated cardiovascular responses are seen in hypovole-mic and hypertensive patients, in whom anesthetic agents abruptly reduce increased sympathetic tone. In addition, patients with “fi xed cardiac output” may demonstrate greater cardiovascular depression during general anesthesia because of an inability to increase cardiac output as systemic vascu-lar resistance decreases.

Positive pressure ventilation is required for many opera-tions and may alter all the determinants of cardiac output, including preload, afterload, heart rate, and contractility. In the absence of hypoxia or hypercapnia, the predominant effects of positive pressure ventilation are mechanical and result from changes in intrathoracic pressure and volume that produce changes in cardiac preload and afterload. During positive pressure inspiration, right atrial pressure (RAP) increases, thereby decreasing right-sided venous return and right ventricular stroke volume. At the same time, left-sided fi lling increases as the pulmonary venous blood is propelled from the pulmonary vasculature toward the left atrium, causing left ventricular (LV) stroke volume to increase. In addition, the increased intrathoracic pressure decreases transmural left ventricular pressure, thereby decreasing LV afterload to further aid LV ejection. Right ventricular (RV) afterload is usually not affected, since the pulmonary circu-lation is contained within the thorax. These phasic changes in intrathoracic pressure and volume produce disparities between right and left ventricular output that vary through-out the respiratory cycle. The predominant effect of positive pressure ventilation results from decreasing systemic venous


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return, producing a form of functional hypovolemia. If large tidal volumes are used in an already hypovolemic patient, venous return can be reduced to a critical level. Thus, the combination of induction of general anesthesia and the institution of mechanical ventilation often requires rapid intravascular volume expansion and vasoactive drug admin-istration to maintain hemodynamic variables within accept-able limits.

Electrocardiography

In high-risk patients, the perioperative period is associated with a signifi cant incidence of dysrhythmias1 and ST-segment changes.2 Intraoperative ECG monitoring is part of routine practice providing the familiar continuous real-time display of one or more standard leads.3 Modern bedside ECG moni-tors are able to record a multilead ECG of diagnostic quality, and computer processing and analysis of the signal aids the detection of ECG changes caused by ischemia or dysrhythmia.

Artifacts and Filters

Electrocardiography monitoring artifacts are common in the operating room environment. Loss of electrical contact of electrodes occurs due to inadequate skin preparation, appli-cation of surgical scrub, or tension on ECG leads. Shivering, tremor, and movements associated with respiration or surgery interfere with the electrical signal and may cause a wander-ing baseline. Equipment commonly used in the operating room may make the ECG uninterpretable (electrocautery), cause a characteristic regular pattern of interference (cardio-pulmonary bypass machines, fl uid warming devices), or produce electrical noise at power mains frequency (60 Hz in North America, 50 Hz in Europe).

Electronic fi ltering of the ECG signal is the standard method used to overcome electrical interference. Many bedside monitors incorporate a monitor fi lter mode that typi-cally has low- and high-frequency fi lters of 0.5 Hz and 40 Hz, respectively. The low-frequency fi lter eliminates baseline drift associated with patient movement, whereas the high-frequency fi lter reduces electrical noise. However, because

the ST segment is a low-frequency component of the ECG, ST-segment shifts may be exaggerated when a low-frequency fi lter of 0.5 Hz is used, leading to overdiagnosis of myocardial ischemia.2,4 The high-frequency fi lter may interfere with QRS recognition, causing the J point to be misidentifi ed and ST segment analysis to be unreliable. A diagnostic fi lter mode now available on most clinical ECG monitors has a similar bandwidth (0.05 Hz to 100 Hz) to a 12-lead ECG machine. This allows the monitored ECG leads to have the same diagnostic accuracy for detection of ischemia as stan-dard ECG recordings. This diagnostic bandwidth fi lter should be used whenever accurate ST-segment analysis is required.

Lead Confi guration

The standard monitoring lead confi guration consists of a fi ve-electrode system, four limb leads, and a single “explor-ing” unipolar precordial electrode. This confi guration allows monitoring of seven of the 12 standard leads (I, II, III, aVR, aVL, aVF, and a single precordial lead). The other precordial leads may be recorded in the operating room by placing the precordial electrode at the standard V1 through V6 positions.

Although the sensitivity of individual ECG leads for detecting intraoperative myocardial ischemia has been extensively studied, there remains some controversy as to whether lead V4 or V5 is the most sensitive in detection of intraoperative ischemic episodes. In a landmark study by London et al.,5 V5 was found to be the most sensitive, fol-lowed by V4, V6, and II (Fig. 119.1). However, a more recent study identifi ed lead V4 as more sensitive.6 The combination of V5 with another lead (II, III, V4, or V6) increases the sensi-tivity of ischemia detection to 90%, with only a small reduc-tion in specifi city. Lead II is commonly monitored along with V5, because it enhances ischemia detection and provides clear evidence of atrial activity, improving dysrhythmia detection.5 A reasonable consensus may be that if only one precordial lead is available, as is the case in most clinical situations, the lead with the most isoelectric ST level out of leads V3, V4, or V5 on the preoperative ECG should be used.6 Most perioperative ST-segment changes of ischemia are seen as ST-segment depression or T-wave inversion resulting from subendocardial ischemia. These changes do not localize the

TABLE 119.1. Cardiovascular effects of anesthetic agents

Systemic vascular Right atrial Mean arterial Cardiac resistance Heart rate Contractility pressure pressure Index

Intravenous induction dose Thiopental − + − − − − − − Midazolam − NC NC NC − NC Propofol − − NC NC − − − − − Etomidate − + − NC − + Ketamine + + + + − + + + + +Inhalational agents at 1 MAC Halothane NC/− NC/− − − + − − − Enfl urane − + − − NC − − − − Isofl urane − − + − NC − − NC/− Sevofl urane −/− − NC NC/− NC − − NC/− Desfl urane −/− − +/+ + NC/− NC − − NC/−

MAC, minimum alveolar concentration; NC, no change; +, minimal increase; ++, marked increase; −, minimal decrease; −−, marked decrease.


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area of ischemic myocardium. Less frequently, ST elevation is observed, suggesting transmural ischemia or infarction in the territory indicated by the respective leads.

Monitoring for myocardial ischemia generally focuses on the left ventricle, but RV ischemia may occur in association with inferior myocardial ischemia or infarction owing to the common blood supply to these areas of myocardium. With the standard monitored combination of leads II and V5, RV ischemia may manifest only as ST elevation in lead II, with or without reciprocal changes of ST depression in lead V5.7 More accurate assessment of RV ischemia is possible with right-sided precordial leads, such as V1 or V4R, the mirror image of the V4 lead on the right side of the chest.8,9

When a three-electrode ECG monitor is the only one available, it may be modifi ed to allow approximation of stan-dard precordial lead positions. Lead I is selected, the positive exploring electrode (left arm) is located in the precordial V5 position, and the central negative electrode (right arm) may be placed in various positions on the thorax to achieve a central subclavicular (CS5), central manubrial (CM5), central chest (CC5), or central back (CB5) lead (Fig. 119.2).

To make valid comparisons of ECG morphology through-out the perioperative period, precordial lead position must be kept constant either by leaving the electrode attached or by marking the skin. Certain types of surgery or positioning

FIGURE 119.1. Single lead sensitivity for detection of myocardial ischemia in noncardiac surgery patients. Fifty-one episodes of intra-operative ischemia were detected in 25 patients using continuous 12-lead electrocardiography. Lead sensitivity was calculated by dividing the number of ischemic episodes detected in a single lead by the total number of episodes detected with all 12 leads. Lead V5 demonstrated the highest single lead sensitivity (75%). Lead II had limited sensitivity (33%). The combination of leads II and V5 increased sensitivity to 80%, and addition of lead V4 increased sen-sitivity to 96%.

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FIGURE 119.2. Modifi cation of the three-electrode bipolar limb lead system to approximate the standard unipolar precordial V5 position. The positive exploring left arm (LA) electrode is placed in the V5 position and the negative central right arm (RA) electrode is

placed in the following locations: central subclavicular (CS), central manubrial (CM), central back (CB) overlying the right scapula, and central chest (CC). Lead I is selected on the monitor to create these modifi ed V5 recordings.



preclude ideal precordial lead selection. For example, left-sided thoracotomy incisions prevent placement of any elec-trodes across the left side of the chest. In addition, despite an anatomically correct surface electrode position, ECG mor-phology and R wave amplitude may be distorted by surgical retraction; movement of the heart within the thorax during prone, sitting, or lateral patient positioning; or by positive pressure ventilation. All of these factors confound intraop-erative ECG interpretation.

Computerized Electrocardiograph Analysis

Computerized ECG processing was originally developed for exercise stress testing, but is now routinely incorporated into bedside monitors. It is useful for noise reduction through signal averaging and for automated ST-segment analysis and trending. The latter feature is most useful, since most epi-sodes of ischemia in the perioperative period pass undetected when an automated system of analysis and recording is not employed.5,10 The fi rst step in processing the ECG signal is conversion of the analog signal into a digital format. The voltage range is divided into a number of discrete measure-ments dependent on the bit size of the microprocessor. Sam-pling rates, typically on the order of 256 Hz and above, result in sampling periods of 4 ms. Low bit size or sampling rate lowers the resolution of the monitor and causes signal distor-tion due to phase shift of the signal. Using mathematical algorithms, fi xed reference points are identifi ed within the signal; for example, the R wave downslope, where there is the most rapid change in signal amplitude. This process allows a baseline QRS complex to be identifi ed and stored as a template with subsequent beats overlaid and averaged. Once the QRS complex or R wave is identifi ed as the refer-ence point, the isoelectric baseline and ST segment measure-ment points are assigned relative to these. For example, for QRS complex identifi cation, the isoelectric point is chosen 40 ms prior to QRS onset and the ST-segment is measured 60 ms after the J-point. For an algorithm based on R wave identifi cation, the isoelectric point is placed 80 ms before and the ST-segment is measured 108 ms after the R wave peak.

Errors may occur when the default setting of the monitor places the isoelectric point or the ST-segment measuring point incorrectly. In cases where there is a short PR interval, the isoelectric point may be placed on the peak of the P wave, producing artifactual ST depression. When a pacing spike is misinterpreted as the R wave peak, both the isoelectric point and the ST segment may be misidentifi ed. Manual adjust-ment of these points may be required.

Computerized interpretation of any ECG abnormality, including ST-segment deviation, always requires confi rma-tion by the physician. However, computer-aided ST-segment analysis allows accurate measurement of ST-segment changes to the nearest 0.01 mV (0.1 mm), thereby alerting the clini-cian to small changes before they reach clinical signifi cance. Some monitors calculate a visual trend line that represents a summation of ST-segment deviations from multiple leads. The sensitivity and specifi city of these bedside monitors in detecting intraoperative ischemia compared to continuous Holter recordings were found to be 74% and 73%, respec-tively.11 Confounding factors included small R waves, wan-dering baselines, conduction abnormalities, and pacing. The

authors emphasized the importance of manually adjusting the ST-segment reference points to ensure accurate compari-son. Computerized ST-segment analysis has also been used to diagnose postoperative myocardial infarction in patients following coronary artery bypass graft surgery.12

In high-risk patients, most intraoperative ST-segment changes occur in the absence of major hemodynamic lability.13–16 Furthermore, control of hemodynamic variables (heart rate and blood pressure) to within 20% of preoperative values does not appear to reduce intraoperative ischemic events.17,18 This poor correlation between hemodynamic control and ischemic ECG changes suggests that it may be a reduction in myocardial oxygen supply rather than increased demand that is most important in development of myocardial ischemia. Strict heart rate control alone during surgery and for the immediate postoperative period (in one study, for 48 hours postoperatively) has been shown to mark-edly reduce the incidence of myocardial ischemia.19 Further-more, it seems that ischemic ECG changes in the postoperative period are more predictive of adverse events compared to preoperative or intraoperative ECG changes.15 It is unclear whether these postoperative changes represent true prognos-tic ability or are part of the ischemic event itself. These observations suggest that, in patients at high risk for adverse cardiac events, ECG monitoring for myocardial ischemia augmented by continuous, computerized ECG monitors, should be continued throughout the early postoperative period, and not just limited to the operating room and recov-ery unit.20

Arterial Blood Pressure Monitoring

Systemic blood pressure represents the necessary driving force generated by left ventricular contraction for perfusion of the body and is the major determinant of left ventricular afterload, the workload of the heart. Consequently, reliable, accurate blood pressure measurement is vital in circum-stances where rapid change is anticipated, such as intraopera-tively and in the critically ill. Standards for intraoperative monitoring require blood pressure measurement at least every 5 minutes,3 and deviation from desired values is often the major indication for pharmacotherapy. Although it seems intuitive that intraoperative blood pressure lability leads to worse outcome, this has not proven to be the case in clinical investigations. This likely results from the rapid detection and early correction of major blood pressure changes during operative procedures.

Direct Measurement of Arterial Blood Pressure

In comparison to noninvasive techniques, direct intraarte-rial blood pressure measurement is more costly and requires additional expertise, but it remains the clinical gold standard as a safe, accurate, and reliable technique. Arterial cannula-tion is considered for two major reasons: frequent arterial blood sampling and pressure measurement. During major surgery, arterial blood analysis guides adjustment of pulmo-nary ventilation and administration of drugs, fl uids, and blood products. New systems have been developed for continuous gas and electrolyte measurement, using either


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fi beroptic sensors placed directly into the artery21 or by an in-line sampling for analysis by ex-vivo sensors.

Direct arterial pressure monitoring is considered when (1) the anticipated hemodynamic change resulting from the operative procedure is sudden or large in magnitude, for example, cardiac or major vascular surgery; (2) concurrent disease necessitates close hemodynamic observation, for example, severe aortic stenosis; (3) pharmacologic or mechan-ical manipulation of the cardiovascular system is planned, for example, intraaortic balloon counterpulsation or deliber-ate hypotension; and (4) cuff-derived pressures are not obtain-able, as in the morbidly obese, burned patient, or severely vasoconstricted patient.22

Components of Direct Blood Pressure Monitoring

Monitoring systems convert mechanical pressure into an easily quantifi able electrical voltage signal that can be dis-played. Mechanical components, such as the intravascular catheter, fl uid-fi lled tubing, and the electromechanical trans-ducer infl uence the signal produced, altering displayed wave-forms and digital values. Faithful re-creation of the arterial pressure waveform requires summation of the fi rst six to ten harmonics derived from Fourier analysis (Fig. 119.3). This is because the arterial waveform contains high frequency com-ponents, such as the systolic upstroke and dicrotic notch. For a pulse rate of 120 beats per minute (2 Hz), the system dynamic response must be fl at to 20 Hz (the tenth harmonic frequency) in order to avoid waveform distortion. The dynamic response of the catheter-transducer system depends on frictional forces, elasticity, and mass, and is characterized by the natural fre-quency and damping coeffi cient of the monitoring system. In an ideal system, input and output signals are identical across the whole range of frequencies, but real systems artifactually amplify the output signal when the input frequency approa-ches the natural resonant frequency of the system. In most catheter-transducer systems, the use of a short length of stiff tubing free of air and clot produces a clinically acceptable natural frequency in excess of 12 Hz.23

The absorption of oscillatory energy by frictional forces is described by the system-damping coeffi cient. An under-

damped system does not dissipate energy, allows exaggera-tion of high- and low-pressure values, and produces artifactual peaks in the waveform. Overdamping causes loss of wave-form detail and a narrowed pulse pressure. Introduction of air bubbles to increase system damping is not recommended, as the natural frequency is also lowered, which may, para-doxically, increase resonance in the system. Optimal damping ensures a fl at frequency response beyond the natural frequency but is diffi cult to achieve.23 Hence, clinical arterial pressure measurement systems behave as underdamped second-order dynamic systems.24

The “fast fl ush test” performed at the bedside assesses the dynamic response of the entire pressure monitoring system (Fig. 119.4).24,25 By quickly opening and closing the fl ush valve, a shock wave is applied to the system, producing a damped oscillation of transducer output. The tighter the oscillation cycles, the higher the natural frequency, and the greater the difference in amplitude of successive oscillations, the more damped the system.

Catheter-tipped transducers circumvent problems of damping and frequency response and can produce very accu-rate measurements. However, they are much more expen-sive, and once placed in the artery, they do not allow transducer drift to be assessed by recalibration. Furthermore, issues of transducer level and hydrostatic infl uences are problematic if not addressed.26 Owing to these limitations, transducer-tipped catheters are not used for routine clinical pressure monitoring.

Modern transducers use semiconductor technology to etch resistor components of a Wheatstone bridge into the surface of the transducer membrane. A standardized sensi-tivity of 5 μV per mm Hg allows exchange of transducers between different monitors. These disposable transducers are highly accurate, incorporate a stiff membrane that pro-duces adequate dynamic range (100–500 Hz), and calibration

FIGURE 119.3. Mathematical reconstruction of the arterial pres-sure waveform. Direct recording of carotid artery pressure is shown by the bold dark blue line (a). A reasonably accurate pressure curve, shown by the dashed red line (b), is reconstructed by summation of the fi rst six harmonics (I, II, III, IV, V, VI) obtained from a Fourier analysis of the original pressure curve.

FIGURE 119.4. Fast fl ush test. The resonant frequency (fn, Hz) cal-culated by dividing the paper speed in millimeters per second by the distance in millimeters between successive oscillation peaks. The amplitude ratio between any two successive peaks (D2/D1) allows the damping coeffi cient to be calculated.



errors and transducer drift are rarely a problem.27 Though calibration is no longer required, a simple calibration check can be performed by raising the tip of the fl uid-fi lled tubing, exposed to air, above the zeroed transducer. The pressure value displayed should correspond with the pressure exerted by the vertical water column acting on the transducer (remembering that 10 cm of H2O pressure equals 7.6 mm Hg).

Perhaps the most common error in pressure measure-ment occurs when the zeroing stopcock is placed at the wrong level with respect to the patient. This reference level should be established at the outset of the monitoring period and checked repeatedly. Although the midaxillary line in a supine patient is usually chosen as the phlebostatic axis, a more accurate point for zeroing the transducer is approxi-mately 5 cm posterior to the sternum. Such a reference point obviates the effect of hydrostatic pressures within the heart chambers.26 Leveling inaccuracies affect all displayed pressures by the same amount, thereby making this a more signifi cant factor for low-pressure systems, such as central venous or pulmonary artery pressures, than for systemic arterial pressures.

The Arterial Waveform

The arterial pressure wave results from the interaction of the forces created by systolic ejection of blood into the vascular tree. The waveform is characterized by a systolic phase—the steep pressure upstroke, peak, and decline until the dicrotic notch—followed by a further decline in the diastolic phase. The impedance and compliance of the arterial tree cause pressure wave refl ection and resonance, progressively trans-forming the central aortic waveform shape as it travels to more peripheral sites. This results in distal pulse wave ampli-fi cation. Other features that distinguish the peripheral arte-rial waveform from central aortic pressure include a dicrotic notch that is delayed and obscured, a refl ected diastolic wave that is more prominent, a systolic peak that is higher, and diastolic nadir that is lower (Fig. 119.5).

Characteristic arterial waveforms are associated with a number of disease states.28 Pulsus alternans, pulsus bis-feriens, pulsus tardus, pulsus paradoxus, and the “spike and dome” pattern seen in hypertrophic cardiomyopathy may be discerned in direct recordings of the system arterial blood pressure just as they are often described in the physical examination of the arterial pulses (Fig. 119.6). In addition, other qualitative circulatory inferences can be gleaned from the waveform shape. A short systolic time is associated with high peripheral resistance or hypovolemia, and a slow systolic upstroke is associated with poor myocardial systolic function, especially in the face of high peripheral resistance.

One commonly used practical application of direct arte-rial blood pressure monitoring is the quantifi cation of the respiratory variation in systolic blood pressure produced during positive pressure ventilation. Excessive variation of the systolic blood pressure (>15 mm Hg) is a strong predictor of occult hypovolemia (Fig. 119.7).29–31 In recent trials, one in patients with sepsis and the other in post–cardiac surgery patients, aortic systolic pressure variation was used to guide volume therapy. In septic, hypotensive patients, systolic pres-

sure variation was a sensitive predictor of patient responsive-ness to volume infusion, and in cardiac surgery patients it predicted an improvement in stroke volume.32,33 It has been suggested that respiratory variation in pulse pressure may be a more useful predictor than variation in peak systolic pres-sure.34 This phenomenon of systolic pressure variation is sometimes visible on a pulse oximetry trace, but owing to the automatic gain adjustment built into these plethysmo-graphic traces, this pulse variation is not a reliable indicator

FIGURE 119.5. Pressure wave refl ection progressively alters the arterial waveform as it travels from the central aorta to the periph-ery. Pulse pressure amplifi cation is noted in the peripheral arterial waveforms.

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FIGURE 119.6. Characteristic peripheral arterial pressure wave-form morphologies associated with pathologic conditions. (A) Normal systemic arterial (ART) and pulmonary artery pressure (PAP) waveforms. (B) The slurred upstroke and delayed systolic peak of aortic stenosis is apparent in comparison with the normal PAP waveform. (C) Aortic regurgitation produces a bisferiens pulse with a widened pulse pressure. (D) The spike and dome pattern of hyper-trophic obstructive cardiomyopathy and the normal waveform (E) following surgical correction. Pressure scales are millimeters mercury. ART scale is on the left, PAP scale is on the right.


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of volume status. There is growing evidence that increased systolic blood pressure variation may be the best indicator of clinically important hypovolemia and fl uid responsiveness, surpassing central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), and even echocardiographically derived left ventricular end-diastolic area.35

Complications of Direct Arterial Pressure Monitoring

As with all invasive monitoring techniques, direct arterial pressure monitoring has an associated morbidity, but com-plications are rare in the absence of contributing factors. In a study of 1700 patients undergoing radial artery cannula-tion, no ischemic complications were demonstrated despite evidence of post-decannulation radial artery occlusion in more than 25% of patients, thus demonstrating the value of collateral circulation provided by the ulnar artery.36 Recana-lization and normalization of blood fl ow usually occurs within 2 weeks.37 Allen’s test is designed to evaluate whether ulnar collateral fl ow is adequate, but its predictive value has been challenged. In many of the reports of ischemic sequelae following cannulation, a normal Allen’s test preceded the arterial catheterization, and in other cases, uncomplicated arterial cannulation occurs even when the Allen’s test is abnormal.36 Overall, the risk of an ischemic complication from peripheral arterial catheterization is less than 0.1%.36,37 Although serious complications are rare following arterial catheterization, reported adverse consequences include infection, fatal hemorrhage, aneurysm formation, arteriove-nous fi stula, retrograde arterial embolism, and compartment syndrome. Of note, the Australia Incident Monitoring Study, which described 2000 perioperative adverse events, reported a lower incidence of complications related to arterial catheterization than either peripheral or central venous cannulation.38

Noninvasive Techniques

In 1896, Scipione Riva-Rocci described the fi rst sphygmoma-nometer that consisted of a cuff encircling the arm and a mercury manometer to measure cuff pressure. The standard method for blood pressure measurement today utilizes the

infl atable occluding cuff and is based on the work of Korot-koff, who described a series of distinct sounds produced by turbulent fl ow during cuff defl ation. For monitoring pur-poses, however, this auscultatory method has a number of limitations. It is highly subjective, labor intensive, and dependent on careful operator technique. Furthermore, reliance on pulsatile blood fl ow for sound generation leads to underestimation of blood pressure in states of low periph-eral blood fl ow,22 whereas hardened atherosclerotic vessels require very high cuff pressures and result in falsely high readings.39

As a result, for repetitive blood pressure monitoring, automatic oscillotonometers have replaced auscultatory techniques. First described by von Recklinghausen in 1936, oscillometry measures cuff pressure changes caused by arte-rial pulsations recorded during cuff defl ation. The point of maximum cuff pressure fl uctuation corresponds to mean arterial pressure, systolic pressure is determined at the point of rapidly increasing oscillations, and diastolic pressure is identifi ed as the point of rapidly decreasing oscillations. In general, values for mean and systolic pressure correspond well with direct arterial pressure measured in the radial artery.40,41 However, discrepancies between indirect oscillo-metric and direct arterial pressures may occur under some conditions, with oscillometry tending to overestimate direct arterial pressure during hypotension and underestimate direct arterial pressure during hypertension.

Although the overall safety of automated blood pressure monitors is underscored by their ubiquitous use in a variety of clinical settings, a number of complications have been reported. These include pain, bruising, limb edema, periph-eral neuropathy, thrombophlebitis, and compartment syndrome.42,43 Risk is increased by frequent or excessive infl ation/defl ation cycling occurring when the “stat” mea-surement mode is used or when repeated cuff infl ations occur in an attempt to overcome artifacts caused by tremor, patient movement, or irregular heart rhythm.

Because automated oscillometric blood pressure mea-surement is intermittent, several techniques have been developed for continuous noninvasive measurement of blood pressure. These include the arterial volume-clamp method using a servo-plethysmomanometer; pulse transit time, using dual oximeters on the ear and fi nger calibrated by oscillom-etry44; arterial wall displacement45; and arterial tonometry using piezoelectric crystals to sense pressure changes trans-duced through a partially fl attened arterial wall.46 In general, these methods show poor agreement with oscillometry or direct arterial blood pressure measurement and have yet to fi nd widespread clinical use as a substitute for direct arterial pressure monitoring.

Central Venous Pressure Monitoring

Central venous catheterization has been used extensively intraoperatively and in intensive care for the past 40 years and continues to expand as new therapeutic indications develop (Table 119.2). Renewed interest in perioperative CVP measurement has gone hand in hand with the continuing debate over the effectiveness of pulmonary artery (PA) cath-eterization. Understanding the physiologic principles under-

120 1 23

1 secΔUp

ΔDown

0

AR

T

FIGURE 119.7. Systolic pressure variation is the difference between maximal and minimal systolic arterial pressures (ART) recorded over the respiratory cycle. A reference end-expiratory baseline value is identifi ed (116 mm Hg, solid horizontal line 1). Total systolic pres-sure variation is the sum of the early inspiratory systolic pressure increase, termed δ up (10.5 mm Hg, line 2) and later decrease in pres-sure, δ down (18.5 mm Hg, line 3) and equals 29 mm Hg. This is much greater than the normal value (5–10 mm Hg). The marked increase in total systolic pressure variation and the exaggerated δ down component suggests the diagnosis of hypovolemia, despite relatively normal blood pressure and heart rate (52 beats/min).


i n t r aop e r at i v e h e mody n a m ic mon i t or i ng 2 52 3

lying CVP monitoring is essential to derive maximum patient benefi t and provides the basis for understanding other waveforms, such as the pulmonary artery wedge pressure (PAWP) and Doppler ultrasound spectral velocity patterns.

Normal Central Venous Pressure

Central venous pressure refl ects the balance between intra-vascular volume, venous tone, and right ventricular func-tion. Central venous pressure is measured in the superior vena cava close to the RA, and for clinical purposes is assumed to equal the right atrial pressure (RAP).

Direct measurement of CVP is often required in high-risk surgical patients. Since assessment by physical examina-tion is often inaccurate,47 and further confounded in the operating room by patient positioning, positive pressure ven-tilation, and the ongoing surgery. In general, a single isolated CVP value provides little information unless it is very high or low. Instead, trends of CVP changes, considered in the context of other hemodynamic variables, prove more clinically useful.

It is important to appreciate mechanical events respon-sible for the characteristic CVP waveform and their relation-ship with ECG activity. The CVP can be considered to possess three systolic components (c wave, x descent, v wave), and two diastolic components (y descent, a wave). Note that fl ow from the vena cavae into the right atrium varies inversely with RAP and is maximal during the x and y pressure descents. These pressure-fl ow relations form the basis for spectral Doppler velocity patterns recorded in the vena cavae or hepatic veins.

Just as careful observation of the arterial pressure wave-form provides useful diagnostic information, interpretation of the CVP waveform yields valuable clinical data. Diagnosis and detection of arrhythmias are enhanced by observing acute changes in the CVP waveform. Junctional (atrioven-tricular nodal) rhythms are common under anesthesia and may cause signifi cant hypotension from a reduction in cardiac output. The hemodynamic clue to this arrhythmia is the CVP cannon a wave, resulting from atrial contraction against a closed tricuspid valve during ventricular systole.

Atrial fi brillation may be recognized in the CVP trace by the absence of a waves and prominent c-v waves. Effective resto-ration of atrioventricular synchrony during pacing can be seen in the CVP wave (Fig. 119.8). Right ventricular (RV) ischemia can produce systemic arterial hypotension and an elevated CVP displaying a prominent a wave resulting from atrial contraction into a stiff right ventricle. If atrial infarc-tion accompanies RV infarction, the a wave is blunted and cardiac output is signifi cantly depressed.48 If tricuspid regur-gitation is present, a tall, regurgitant c-v wave further increases mean CVP.

TABLE 119.2. Indications for central venous catheterization

Central venous pressure monitoringPulmonary artery catheterization and monitoringDrug administration Vasoactive drugs Hyperosmolar fl uids Chemotherapy agents Prolonged antibiotic therapy Drugs acting primarily on the pulmonary circulationParenteral nutritionRapid fl uid infusionTemporary transvenous pacingHemodialysisPortosystemic shunt insertionAspiration of air emboliInadequate peripheral venous accessRepeated blood sampling

20

A

B

C

CVP

CVP

R

RR

R R

a

1 sec

1 sec

1 sec

c v

y10

0

20

10

0

0

0

ART

CVP

f f fc v

y

100

200

15

f f f

FIGURE 119.8. (A) Atrial fi brillation obliterates the central venous pressure a wave, augments the c wave, and preserves the v wave and y descent. (B) Junctional rhythm causes atrial contraction against a closed tricuspid valve to produce tall early systolic cannon a waves (*) that occur after the electrocardiography R wave (right). Compare with sinus rhythm (left). (C) Fibrillation/fl utter (f) waves apparent in the CVP trace assist in diagnosis of the underlying atrial arrhyth-mia. The CVP c and v waves and the dominant y descent are noted.


2 52 4 c h a p t e r 119

Pericardial constriction restricts venous return to the heart and increases CVP. The a and v waves are prominent and the x and y descents are steep, creating an M or W pattern, similar to RV infarction or other conditions in which right ventricular compliance is reduced. The CVP y descent is halted abruptly as diastolic infl ow into the RV is restricted, producing a diastolic pressure plateau (the h wave) and creat-ing a pattern termed “dip and plateau” or “square root sign” (Fig. 119.9).

As in pericardial constriction, the CVP in cardiac tam-ponade is increased and there is end-diastolic pressure equal-ization in all four cardiac chambers. However, in contrast to pericardial constriction, tamponade couples atrial and ven-tricular volume changes and produces a CVP waveform that is distinguished by the attenuated y descent.49

Complications

Complications can be divided into those resulting from attempts at gaining central vascular access or from the pres-ence of the CVP catheter in the body (Table 119.3). Serious complications have been described at each vascular access location. Unintended arterial puncture is the most common complication. Experienced operators and the use of ultra-sound to locate the central vein reduce this risk. If cannula-tion of the carotid artery occurs, there is signifi cant risk of hematoma formation compromising airway patency. Contro-versy exists over whether to remove the catheter from the artery and apply local pressure or whether the catheter should be left in situ and removed only after vascular surgical consultation, neck exploration, and vessel repair.

Recent development of small, portable ultrasound machines has made it possible to image the great veins of the neck prior to or during placement of central venous cath-eters. This has been shown in multiple clinical studies as well as in a recent meta-analysis to decrease the incidence of failed catheter placement as well as the complication rate, especially in high-risk patients.50–53 Routine use has been

recommended, although practitioners must maintain skills in the landmark method, as ultrasound machines may not be available in emergency situations.50,54 Economic modeling has shown that use of ultrasound is likely to save $3249 for each 1000 catheters placed.54

Pulmonary Artery Catheterization

Since its introduction into clinical practice in the 1970s for treatment of patients with acute myocardial infarction,55 the pulmonary artery catheter (PAC) has been accepted as an important monitoring device for high-risk surgical and criti-cally ill patients. Pulmonary artery catheters allow measure-ment of intracardiac pressures, cardiac output (CO), mixed venous oxygen saturation, and RV ejection fraction. Along with intracardiac and mixed venous blood samples, these PAC-derived measurements allow calculation of hemody-namic indices and shunt ratios and provide data that are not obtainable by any other means.56 This information may be helpful in diagnosing and managing rapidly varying hemo-dynamic changes and guiding fl uid and vasoactive drug therapy. However, despite widespread use of the PAC for the past three decades, controversy concerning its clinical role remains.57–61 Not only have PACs not been shown to result in improved outcome in many of the conditions in which they are used,62–64 but some studies have suggested increased harm.65–68

R R R 1 sec

200

0

20

0

ART

CVPa

a

ac v

vv

h

hy

y

x

x

TABLE 119.3. Complications of central venous catheterization

From gaining venous access and cannulationArterial puncture Hematoma Hemothorax Arterial thromboembolism Arterial cannulationAirway obstructionNerve and brachial plexus injuryTracheal and laryngeal traumaChylothoraxPneumothoraxSubcutaneous, mediastinal emphysemaAir embolismCatheter or wire shearing and embolizationFrom catheter presenceVenous thrombosis and thromboembolism Superior vena cava syndrome Pulmonary embolismInfection Cellulitis Sepsis EndocarditisArrhythmiasVascular injury Arteriovenous fi stula Aortoatrial fi stula Venobronchial fi stula Perforation of superior vena cava, right atrium, right ventricle Cardiac tamponadeHydrothorax/hydromediastinum

FIGURE 119.9. Pericardial constriction causes increased central venous pressure with tall a and v waves, steep x and y descents, and a mid-diastolic plateau (h) wave. Pericardiectomy produces resolu-tion of the pathologic CVP waveform. These changes are noted in the progression of panels from left to right. The steep y descent and h wave pressure plateau are analogous to the “square root sign” seen in the ventricular pressure trace of this condition. The arterial blood pressure (ART) waveform is shown to highlight waveform timing.



If PAC monitoring is to provide any benefi t to patients, clinicians using these catheters must be aware of the methods, indications, and complications of insertion, and understand the physiologic and technical principles involved. Only by correctly interpreting and appropriately applying data obtained with continual hemodynamic monitoring, will the PAC be fully exploited to provide maximum patient benefi t.

Practical Considerations for Insertion

The right internal jugular vein is the most commonly chosen route of central venous access for PAC placement as it affords the most direct path between puncture site and the heart. As the catheter is advanced from the internal jugular insertion site, the RA is encountered at 20 to 25 cm, RV at 25 to 35 cm, PA at 35 to 45 cm, and the wedge position at approximately 50 cm.69 By keeping these estimated distances in mind, the clinician can avoid excessive catheter insertion that may lead to catheter coiling or knotting within the heart. The subclavian route of insertion is associated with a higher incidence of pneumothorax, a particularly dangerous compli-cation in patients receiving positive pressure ventilation. From more peripheral sites, such as the femoral vein, the PAC may be more diffi cult to position correctly or adjust intraoperatively when there is limited access to the patient. Because the PAC is balloon-tipped and fl ow-guided, patient positioning infl uences the ease with which it passes through the heart. A combined head up/right-side down positioning aids fl otation across the pulmonic valve.70 The head-down (Trendelenburg) position should be avoided as it is associated with more severe dysrhythmias during insertion.71

A large increase in systolic pressure occurs with passage of the PAC from RA to RV, followed by a diastolic pressure step up that signifi es that the catheter has entered the PA. Rather than digital readouts alone, a real-time pressure waveform display is required to identify intravascular cath-eter tip position. For example, a pressure of 30/10 mm Hg is diffi cult to interpret and may be recorded from the RV or the PA. Observing the pressure tracing clarifi es the matter, as the PA pressure wave has a dicrotic notch with pressure falling steadily from the systolic pressure peak until the next pressure upstroke, whereas the pressure recorded in the RV gradually rises in diastole as the ventricle fi lls until onset of systole (Fig. 119.10).

Complications

Complications associated with PA catheterization arise from the required central venous cannulation, initial catheter placement and positioning, the continued presence of the catheter within the body, misuse of equipment, or misinter-pretation of catheter-derived data. The reported frequency of complications varies greatly and is diffi cult to determine accurately, as most complications are described in case reports or small case series.72,73 Minor complications, such as self-limited arrhythmias, occur in up to 50% of insertions, but serious life-threatening complications are rarer, occur-ring in 1.5% to 10% of catheterized patients. Death attribut-able to PAC insertion and use is reported in 0.02% to 1.5% of patients.73 A large prospective study of 6245 catheteriza-tions of cardiac and noncardiac surgical patients reported

catheter-related serious morbidity in 0.16% and mortality in 0.016% of patients.74 The authors suggested that expertise and experience of the attending physician, close supervision of trainees, and attention to detail were factors that mini-mized complications.

Arrhythmias

Although transient arrhythmias, most commonly premature ventricular contractions (PVCs), frequently accompany passage of the PAC through the heart, complete heart block, ventricular tachycardia, and ventricular fi brillation have been reported. Shah et al.74 observed that 68% of patients experienced PVCs, with only 3.1% requiring treatment. Pro-phylactic lidocaine to suppress catheter-related arrhythmias is of questionable effi cacy.75 Since transient right bundle branch block occurs during catheterization in up to 5% of patients,76–78 complete heart block may be precipitated in patients with preexisting left bundle branch block.79 However, as this happens rarely,74,76 prophylactic placement of a trans-venous pacing wire is not warranted. Instead, transcutaneous pacing should be available or a pacing PAC should be chosen.

Catheter Knotting

Coiling, looping, and knotting of catheters within the heart has been described and is more likely in low cardiac output states, when the heart chambers are dilated, and when the catheter is advanced to excessive distances.80,81 Intracardiac pacing wires or anatomic structures, such as chordae tendin-eae, may become entangled in PACs.82,83 Catheter knots may be disentangled under fl uoroscopic guidance using intravas-cular snares,84,85 or they may be pulled tight and removed with the catheter sheath. If these methods fail or the catheter is entrapped in a cardiac structure, surgical removal is required.

Valvular Damage, Endocarditis, and Thromboembolism

The PAC balloon must be completely defl ated prior to catheter withdrawal to avoid damage to the tricuspid86 or

30

0Right atrium Right ventricle Pulmonary artery Wedge

RRRRa c v va-c

1 sec

FIGURE 119.10. Characteristic pressure waveforms recorded during passage of a pulmonary artery catheter. The right atrial pressure trace displays the a, c, and v waves seen in a normal central venous pressure recording. Right ventricular pressure demonstrates the increase in systolic pressure; however, end-diastolic pressure is the same as in the right atrium and is best estimated by the right atrial pressure a wave peak. Increasing right ventricular pressure during diastole in contrast to the decreasing pulmonary artery pressure (shaded boxes) helps to differentiate these recordings. Pulmonary artery wedge pressure has a venous pressure morphology similar to right atrial pressure, but the a, c, and v waves appear delayed in relation to the electrocardiography.


2 52 6 c h a p t e r 119

pulmonary valves.87 Despite proper catheter management, occult endocardial damage occurs frequently and may result in endocarditis.88–91

Minor thrombi associated with PACs were common, but have been markedly reduced by the use of heparin-bonded catheters.92 While major thromboembolism associated with PAC use remains rare, a recent large study has shown a 0.9% incidence of pulmonary embolism in patients randomized to PAC-guided therapy versus none in the control group.64 The PAC lumina must always be fl ushed continuously with a crystalloid solution, but addition of heparin to the fl ush in an attempt to reduce thrombotic complications has not been shown to be effective and may induce thrombocytopenia.93

Catheter-Related Infections

While bacteremia may produce catheter colonization, cath-eter-related infection more often results from skin organisms colonizing the introducer sheath.94 Mermel et al.95 demon-strated a 22% incidence of local infection of the introducer sheath but only 0.7% incidence of PAC-associated bactere-mia. Another study has shown a similar infection rate between heparin-bonded PACs and regular central venous catheters (2.6 infections per 1000 catheter days), while non–heparin-bonded catheters had shown a higher infection rate (5.5 per 1000 catheter days).96 Leaving the PAC in place for more than 5 to 7 days also increases the risk of infection; however, no data exist to suggest that routine replacement of catheters is advantageous.96 Guidelines for prevention of catheter-related infections were recently developed and are summarized in Table 119.4.

Pulmonary Vascular Injury

Pulmonary vascular injury is a rare but potentially life-threatening complication of PA catheterization. Pulmonary infarction may result from prolonged balloon infl ation or distal catheter migration.97 Of even greater concern, PA rupture may occur with an incidence of 0.02% to 2.0% and mortality of 40% to 70%.64,98–100 Hemoptysis is the cardinal sign, and advanced age, anticoagulation, and pulmonary hypertension are common, albeit unproven, associations.99–101

Treatment focuses on maintaining oxygenation and control of bleeding. Endobronchial intubation with either a single- or double-lumen endotracheal tube allows selective lung ventilation and isolates the bleeding segment.102 Other treatments include antihypertensive therapy to lower PA pressure, reversing anticoagulation, and bronchoscopy for

endobronchial toilet and identifi cation of the site of bleeding. Although transcatheter embolization by steel coil103 or tissue-adhesive occlusive agent104 may control hemorrhage, surgical lung resection is required when conservative treat-ment fails,98,100 or if life-threatening hemothorax develops.100 Pseudoaneurysm has been reported as a late complication that may require further treatment in patients initially treated conservatively.98

Data Interpretation Errors

Perhaps the most common complication of the PAC is an insidious one—the misinterpretation of hemodynamic data. Several investigators have shown a poor level of knowledge among users of PACs, including nurses, physicians, and spe-cialists in critical care medicine.105–107 A fundamental skill, waveform interpretation, is performed inconsistently even by experienced physicians.105–108 Even when given the same PAC data, experienced intensivists differ markedly in its interpretation and the choice of intervention, highlighting the extreme diffi culty in evaluating PAC outcome studies.109 Clearly, skilled use of the PAC is a basic requirement if cath-eterization is to have any benefi t. These training require-ments are well outlined by the American College of Cardiology, Society of Critical Care Medicine, and the Amer-ican Society of Anesthesiologists Task Forces.73,110,111 A recent National Institutes of Health (NIH)-sponsored consensus statement had identifi ed developing a standardized educa-tional program as its most important recommendation.112

Pulmonary Artery Occlusion Pressure

When the PAC catheter is fl oated to a wedged position, a static column of blood connects the catheter tip to a junction point where fl ow resumes in the pulmonary veins near the left atrium (LA).113 Since resistance to fl ow in the large pul-monary veins is low, pulmonary artery occlusion presence (PAOP) provides an accurate estimate for pulmonary venous pressure (PVP) and left atrial pressure (LAP). In addition, the same phasic mechanical events that generate the CVP waves (a, c, and v) create a similar waveform pattern in the LAP and PAOP waveforms. Consequently, the PAOP tracing may be recognized by characteristic a, c, and v waves that refl ect a LAP waveform that is slightly delayed and damped by the interposed pulmonary vascular bed. Owing to these ana-tomic factors, the PAOP a wave appears after the ECG R wave, even though it refl ects end-diastolic left atrial contrac-tion. Pulmonary artery wedge pressure is usually reported as a single mean value for assessing the hydrostatic back-pressure that infl uences pulmonary edema formation. As a predictor of LV preload, however, the phasic PAOP recorded at the peak of the a wave provides a better estimate of left ventricular end-diastolic pressure (LVEDP), particularly in patients with LV dysfunction.114 Although some authors use the term pulmonary capillary pressure interchangeably with PAOP, capillary pressure is usually slightly higher than PAOP and may be signifi cantly higher when pulmonary venous resistance is elevated.113 The true pulmonary capil-lary pressure, which is the pressure driving the creation of interstitial pulmonary edema, can be derived from the pres-sure decay curve following PAC balloon infl ation.115,116

TABLE 119.4. Guidelines for prevention of catheter-related infections96

Education and training of physicians and nursesAvoidance of femoral vein catheterizationUsing full sterile technique for catheter insertion (including cap, mask, gown, sterile gloves and drapes)Skin antisepsis with chlorhexidine 2% solution rather than povidone-iodineUse of heparin-bonded cathetersAs short as possible duration of use



Factors Affecting Data Validity

Many factors can adversely affect the accuracy of the data collected from the PAC.117 In the assessment of LV preload, the further “upstream” from the LV that pressures are mea-sured, the more prone is the estimate to confounding errors. These and other variables affecting the accuracy of the PAOP are discussed herein and are summarized in Table 119.5.

Pulmonary Artery Catheter Artifacts

Motion of the PAC induced by cardiac contraction creates artifactual spikes or troughs in the pulmonary artery pressure (PAP) waveform. These catheter fl ing artifacts are observed often following the ECG R wave when tricuspid valve closure and ventricular contraction set the PAC in motion (Fig. 119.11). Another pressure artifact, termed “over-wedging,” is produced when a gradually rising, nonpulsatile pressure is recorded after balloon infl ation. This occurs when the catheter tip is forced against the wall of the PA, occluding the PA lumen of the PAC so that pressure builds from the continuous pressurized fl ush system. When this problem is

suspected, immediate balloon defl ation followed by PAC withdrawing and repositioning is mandatory to reduce the risk of PA rupture.

Catheter Tip Position and Respiratory Infl uences

West et al.118 characterized gravity-dependent differences in lung perfusion and ventilation depending on the relationship of pulmonary arterial pressure (Pa), alveolar pressure (Palv), and pulmonary venous pressure (Pv).118 In lung zone 1, Palv exceeds both Pa and Pv, in zone 2 Palv exceeds Pv but not Pa, and in zone 3 Pa and Pv exceed Palv. Consequently, zone 3 conditions must be present in the portion of the lung con-taining the PAC for the PAOP to provide a valid estimate of LAP (Fig. 119.12). Alveolar rather than intravascular pres-sures are measured when the catheter tip is located in zone

TABLE 119.5. Underestimation and overestimation of left ventricular end-diastolic pressure

Condition Site of discrepancy Cause of discrepancy

UnderestimationDecreased left ventricular compliance Mean LAP < LVEDP Increased end-diastolic a waveAortic regurgitation LAP a wave < LVEDP Mitral valve closure prior to end-diastolePulmonic regurgitation PADP < LVEDP Bidirectional runoff for pulmonary artery fl owRight bundle branch block PADP < LVEDP Delayed pulmonic valve openingDecreased pulmonary vascular bed PAOP < LVEDP Obstruction of pulmonary blood fl owOverestimationPositive end-expiratory pressure Mean PAOP > Mean LAP Creation of lung zone 1 or 2 or pericardial pressure changesPulmonary arterial hypertension PADP > Mean PAOP Increased pulmonary vascular resistancePulmonary veno-occlusive disease Mean PAOP > Mean LAP Obstruction to fl ow in large pulmonary veinsMitral stenosis Mean LAP > LVEDP Obstruction to fl ow across mitral valveMitral regurgitation Mean LAP > LVEDP Retrograde systolic v wave raises mean atrial pressureVentricular septal defect Mean LAP > LVEDP Antegrade systolic v wave raises mean atrial pressureTachycardia PADP > Mean LAP > LVEDP Short diastole creates pulmonary vascular and mitral valve

gradients

LVEDP, left ventricular end-diastolic pressure; PADP, pulmonary artery diastolic pressure; PAOP, pulmonary artery occlusion pressure; LAP, left atrial pressure.

30

0

A

B

1 sec PAP 28/0

FIGURE 119.11. Artifactual pressure peaks and troughs in the pul-monary artery pressure (PAP) trace appear following the electrocar-diography R wave and result from motion of the pulmonary artery catheter. The correct value for end-diastolic PAP is 8 mm Hg (A), although the monitor displays an artifactual value of 0 mm Hg (PAP 28/0 mm Hg, B).

PA

Zone 1

Zone 1 PA > Pa > Pv

Zone 2 Pa > PA > Pv

Zone 3 Pa > Pv > PA

Zone 2

Zone 3

LA

LV

Pa

RA

RV

Pv

FIGURE 119.12. The pulmonary artery (PA) catheter tip must be wedged in the most dependent part of the lung, zone 3 to measure accurately pulmonary venous (Pv) or left atrial (LA) pressure. When alveolar pressure (PA) rises above Pv in zone 2 or above pulmonary arterial (Pa) pressure in zone 1, wedge pressure refl ects alveolar rather than intravascular pressures. RA, right atrium; RV, right ventricle; LV, left ventricle.


2 52 8 c h a p t e r 119

1 or 2. This may be suspected when the PAOP trace does not have characteristic a and v waves and when there is excessive respiratory variation in the trace.

Pulmonary Vascular Resistance and Heart Rate

Since normal pulmonary vascular resistance (PVR) is low, pulmonary blood fl ow ceases at end-diastole, and PA dia-stolic pressure (PADP) equals LAP. If PVR is elevated, pul-monary blood fl ow continues throughout the cardiac cycle, and a pressure gradient remains between PA and LA at end-diastole. In this case, PADP overestimates downstream LAP or LVEDP, but PAOP remains an accurate estimate for LVEDP because there is no pressure gradient across the static column of blood connecting the wedged catheter tip to the junction point in the pulmonary veins. Pulmonary artery diastolic pressure also may overestimate LAP in pulmonary veno-occlusive disease if the site of venous occlusion involves the large pulmonary veins.119,120

When the pulmonary vascular bed is reduced after pneu-monectomy or large pulmonary embolus, PAC balloon infl a-tion itself may cause signifi cant obstruction of pulmonary blood fl ow, reducing LAP while simultaneously increasing PAP.121 In these conditions, PAOP measurement artifactually decreases LV preload, so that the PAOP value recorded under-estimates true LV fi lling pressure.

As the duration of diastole shortens with increasing heart rate, the time for fl ow across the pulmonary bed decreases, producing a diastolic pressure gradient between PAP and LAP similar to that seen in pulmonary hypertension.122 This effect of tachycardia is greatest when PVR is elevated. Tachy-cardia may also produce a pressure gradient across the mitral valve, resulting in LAP exceeding LVEDP.

Valvular Disease

When there is signifi cant pulmonary valve regurgitation and RV diastolic pressure is lower than LAP, PAP seeks the lower pressure value at end-diastole, and PADP (but not PAOP) will be lower than LAP and underestimate LVEDP. With aortic valve regurgitation, diastolic fi lling of the LV occurs as soon as LV pressure falls below aortic root pressure and continues after mitral valve closure. Consequently, PADP, PAWP, and LAP underestimate LVEDP. With mitral stenosis, a pressure gradient from LA to LV exists throughout diastole, causing the PAOP and LAP to overestimate LVEDP. Mitral regurgita-tion produces tall regurgitant c-v waves in the PAWP trace, increasing mean LAP and the risk of pulmonary edema. Rather than the normal late systolic v wave caused by venous fi lling of the atrium, the combined c-v wave begins in early ventricular systole. Mean PAOP will increase and overesti-mate LVEDP, which is better estimated in these patients by the pressure value recorded before onset of the c-v wave. Thus, mean PAOP accurately estimates mean LAP in mitral valve disease, but overestimates LVEDP. The height of the c-v wave in the PAOP trace has not been found to accurately refl ect the severity of mitral regurgitation.123 It depends not only on the volume of regurgitation, but also on LA compli-ance and volume.124 For example, large c-v waves are often present in acute mitral regurgitation, whereas a similar degree of regurgitation in chronic mitral regurgitation does not produce a tall c-v wave.125

Ventilatory Pressure Infl uences

The net distending pressure responsible for diastolic fi lling of the heart is best described by transmural pressure (LVEDP – intrapericardial pressure). During large swings in intratho-racic pressures, as in labored respiration, coughing, Valsalva maneuver, and positive pressure ventilation, both the intra-cardiac and intrapericardial pressures are affected, but only the intracardiac pressures are measured through the PAC. Consequently, spurious changes in LVEDP will be detected, not refl ecting the true transmural pressure and, consequently, the true preload.120,126 The best way to obviate these con-founding effects of intrathoracic pressure change is to measure intravascular pressures at end-expiration. At this point in the respiratory cycle, intrathoracic pressure approxi-mates atmospheric pressure, whether the patient is breathing spontaneously or mechanically ventilated. Under these cir-cumstances, central vascular and intracardiac pressures measured at end-expiration will provide the best estimate for transmural fi lling pressures. Visual inspection of the wave-form display is the most accurate method for identifying end-expiratory pressures. Reliance on digital displays should be avoided, since these are notoriously inaccurate.127

The identifi cation of end-expiration may be diffi cult when patients on mechanical ventilation have vigorous respiratory muscle activity, as the inspiratory triggering may reduce the airway pressure and the measured PAOP below end-expiration levels. Muscle relaxation will allow more accurate estimation of the true PAOP in this setting.128

Another confounding assumption in PAC pressure mea-surements is that the end-expiratory intrathoracic pressure is always zero. Clearly, this is not true in the setting of positive end-expiratory pressure (PEEP).113 The degree to which PEEP alters intrathoracic and intrapericardial pressures (and hence PAOP) depends on pulmonary and chest wall compliance. The PEEP usually increases measured PAOP less than one half the value of PEEP applied. Fortunately, high levels of PEEP are usually only required when pulmonary compliance is mark-edly reduced, which attenuates the transmission of these high airway pressures to the pleural space.120,129 Prolonged airway disconnection obviates the effect of PEEP on PAC measure-ments, but may alter venous return and other hemodynamic values and have a deleterious effect on respiratory mechanics and gas exchange. As an alternative, transient airway discon-nection from mechanical ventilation with PEEP for less than 3 seconds may allow estimation of the infl uence of high levels of PEEP with a greater margin of safety.130

Another way to eliminate the effect of PEEP is to calcu-late an index of airway pressure transmission as follows: (End-inspiratory PAOP – End-expiratory PAOP)/(Ventilatory plateau pressure – PEEP). Then the true PAOP can be calcu-lated as measured end-expiratory PAOP minus the index of transmission multiplied by the PEEP level.131 One advantage of this technique is that it applies also to patients with dynamic hyperinfl ation [e.g., patients with signifi cant chronic obstructive pulmonary disease (COPD) or adult respiratory distress syndrome (ARDS)], where lung volume does not quickly return to functional residual capacity on disconnection from the ventilator. The PEEP level used to make the calculations should be the total PEEP, including the occult or auto-PEEP.131



Ventricular Compliance and Pressure Volume Relationships

Since the pressure-volume relationship of the LV is curvilin-ear, changes in LVEDP can result from small or large changes in ventricular volume depending on the portion of the com-pliance curve over which the LV is operating. Conditions causing a marked shift in the compliance curve may result in pressure and volume changing in opposite directions, that is, decreased fi lling pressure associated with increased left ventricular volume.132 These physiologic considerations further complicate interpretation of PADP, PAOP, LAP, or LVEDP as measures of LV preload. The ventricular pressure-volume relation is infl uenced by both intrinsic factors, such as wall thickness, chamber size, and passive and active relax-ation, and extrinsic factors, such as pericardial pressure, intrathoracic pressure, and ventricular interdependence. In the perioperative period, processes, such as myocardial isch-emia, pulmonary hypertension with right ventricular failure, and inotropic drug effects, can all induce rapid changes in LV compliance.

Clinical Uses of the Pulmonary Artery Catheter in the Perioperative Period

Cardiac Preload

One of the primary reasons for PAC monitoring is to provide an estimate of LV preload. The assumption is that increasing preload will translate into an increase in cardiac output (Star-ling effect), improving tissue perfusion. In clinical practice, true preload, that is, LV end-diastolic volume, is not readily available, and pressure surrogates are used instead. Usually, PAOP below 10 mm Hg is considered a marker of hypovole-mia, while PAOP >18 mm Hg suggest fully distended LV.133 However, a study in patients undergoing cardiac surgery has demonstrated that for the same LVEDV, patients with LV hypertrophy have higher PAOP. When LVEDV was optimized with repeated fl uid boluses, PAOP in these patients was fre-quently higher than 20 mm Hg.134 Indeed, considering all the factors discussed above that can adversely affect PAOP accu-racy, it is not surprising that clinical studies have repeatedly shown poor correlation between the absolute PAOP numbers and either LVEDV135 or the cardiac output response to fl uid challenge.32,136,137 One practical approach is to administer a rapid “fl uid challenge” (250 mL) over 10 minutes while moni-toring the change in PAOP and other hemodynamic vari-ables. A large change in PAOP (greater than 7 mm Hg) means that the LV is operating on the steep portion of its compli-ance curve and further fl uid administration will risk pul-monary edema and an increase in myocardial oxygen consumption without increasing stroke volume and cardiac output.120 In contrast, a small increase in PAOP (less than 3 mm Hg) suggests that further volume administration may be benefi cial in improving stroke volume. While practical, no outcome studies have validated this approach.

Pulmonary Edema

Traditionally, a pulmonary capillary pressure of above 18 to 20 mm Hg is considered to promote alveolar fl ooding.138 Similarly, a pulmonary artery occlusive pressure of below

18 mm Hg is used to classify pulmonary edema into a non-cardiogenic versus cardiogenic etiologies.139 In clinical appli-cations, the PAOP is used as a surrogate for pulmonary capillary pressure, assuming negligible pulmonary venous resistance. When optimizing preload, it might be prudent to keep the PAOP less than 18 to 20 mm Hg to decrease the risk of pulmonary edema. However, in patients with acute lung injury and leaky capillaries, as commonly seen periopera-tively in settings of ischemia-reperfusion or sepsis, even lower capillary pressures may be associated with increased pulmonary edema, suggesting that there might not be a safe level of PAOP.140 On the other hand, as discussed above, posi-tive pressure ventilation may spuriously increase the PAOP to levels above 18 mm Hg while simultaneously increasing the interstitial tissue pressure without net increase in the fi ltration pressure gradient. The potential pressure gradient between PAOP and true pulmonary capillary pressure in situations where pulmonary venous resistance increases (e.g., sepsis, ARDS) also detracts from the usefulness of PAOP as an indicator of risk for formation of pulmonary edema.

Goal-Directed Therapy

In high-risk surgical patients, some evidence suggests that perioperative “optimization” of oxygen delivery and cardiac index with fl uids, blood, and inotropes to achieve predeter-mined physiologic values (e.g., oxygen delivery around 600 mL/min/m2, cardiac index greater than 3.5 to 4 L/min/m2, mixed venous saturation >70%) may reduce mortality, complications, and hospital length of stay.141–145 This type of treatment, preemptively instituted in the intensive care unit and the operating room in patients who are not yet critically ill, has been termed early goal-directed therapy. A similar approach has been found to be benefi cial in nonsurgical patients with early stages of sepsis.146 In contrast, more delayed institution of a goal-directed therapy in critically ill medical and surgical patients who have an established sys-temic infl ammatory response syndrome or severe organ dys-function has not been shown to lead to improved outcome.147,148 In the largest randomized study to date, testing early goal-directed therapy in high-risk surgical patients, however, no benefi t was demonstrated in the treatment group.64

Several studies have examined the role of fl uid-based goal-directed therapies in surgical patients and have found better outcome in the treatment groups.149–151 As these last mentioned studies demonstrate, goal-directed therapy as a treatment protocol does not rely on the use of the PAC, as goals can be set and therapy directed using other types of monitors (e.g., esophageal Doppler, central venous oximetry).

Detection of Myocardial Ischemia

The physiologic changes of myocardial ischemia can be detected with a PAC. Ischemia-induced diastolic dysfunction increases mean PAOP and the phasic a and v waves become more prominent. Although PADP and PAOP often increase during ischemia, this does not necessarily indicate increased LV preload.152,153 Diastolic LV dysfunction, particularly char-acteristic of demand-induced ischemia, impairs LV relax-ation. In these patients, LVEDP may be estimated best by the a wave pressure peak rather than the mean PAWP. In addi-tion, ischemia may lead to acute mitral valve regurgitation


2 53 0 c h a p t e r 119

and a tall systolic c-v wave in the wedge trace.154 Although the above changes have been described in patients undergo-ing surgery, changes in PAOP may be small and diffi cult to detect clinically. Furthermore, there is no quantitative threshold value for mean PAOP, change in PAOP, or PAOP a or v wave height that is diagnostic of myocardial ischemia. In general, there is poor agreement among ECG, PAC, and echocardiographic indicators of myocardial ischemia when these variables are all monitored simultaneously during surgery.155,156 This limits the use of the PAC as a primary monitor for ischemia.

The Evidence For and Against the Pulmonary Artery Catheter

Which conditions warrant PAC placement are largely infl u-enced by institutional, geographical,157 organizational,158 and individual preferences.159 Widespread dissemination of PAC monitoring occurred before this technology was evaluated rigorously. Studies showing no benefi t or worse outcome associated with PAC monitoring,63,68,147,148,160–166 and studies supporting its use,141,142,144,145,167–169 provide confl icting evi-dence. A major problem with evaluating the results from most of the studies have been inadequate study methodology, unequal case mix, and small sample size.73,110 Recently, several larger, better designed studies have been published examining the value of routine use of the PAC in periopera-tive medicine: One large observational study has shown that the use of PAC in major noncardiac surgery was associated with an independent 2.2-fold increase in risk of cardiac com-plications.67 In moderate-risk vascular surgery, both a ran-domized controlled study66 and a meta-analysis170 have shown lack of benefi t associated with PAC use. Another large (n = 1994) randomized study that tested the use of the PAC in elderly high-risk surgical patients found no benefi t, but no excess mortality, in the PAC group.64 Lastly, a large prospec-tive randomized study in patients undergoing coronary artery bypass surgery have shown no benefi t in routine use of the PAC compared with CVP monitoring.171 It should be noted, however, that all of these studies have tested the routine use of PAC in a large sequential cohort of patients with a rela-tively low to moderate risk of death.61 As some data suggest, PAC may be benefi cial in especially high-risk patients with high level of disease acuity.172 Also, few data exist regarding the use of PAC as a “rescue” monitor in patients who have developed refractory hemodynamic derangements perioperatively.173

In the absence of convincing outcome studies, several expert panels have tried to provide practice guidelines acknowledging these uncertainties but aiming to help stan-dardize clinical practice.73,110–112 Specifi cally aiming at the perioperative period, the American Society of Anesthesiolo-gists (ASA) task force recently renewed its recommendations for PAC usage based on analysis of the current literature as well as expert opinion.73 The delay associated with PAC placement after complications have developed, as well as possibly increased vascular and septic complications related to hasty insertion under less than ideal conditions, suggest that preemptive PAC insertion in patients deemed at high risk is a justifi able practice.73 Operator experience plays a

signifi cant role in preventing PAC complications, and better physician knowledge and understanding of the physiologic principles behind the numbers might contribute immensely to PAC effectiveness.106,109 According to the ASA task force, the use of PAC is considered necessary only in high-risk patients undergoing high-risk surgery, and under the condi-tion that the practice environment is favorable (i.e., knowl-edgeable and experienced physicians and ICU nurses). High-risk patients are generally in ASA class 4 or 5 and have signifi cant cardiovascular disease, pulmonary dysfunction, renal insuffi ciency, sepsis, or trauma. High-risk surgery includes procedures commonly associated with large fl uid shifts or hemodynamic derangements as well as with high mortality. The task force does recognize that PAC use may still be considered appropriate even in less risky combina-tions of moderate-risk patients (i.e., ASA class 3) undergoing high-risk surgery, or high-risk patients undergoing moderate-risk surgery.73 It should also be stressed that alternative monitoring techniques, especially transesophageal echocar-diography (vide infra), can rapidly supplant the use of the PAC in many situations.174

Special Types of Pulmonary Artery Catheter

Pacing Pulmonary Artery Catheter

Multipurpose PACs allow cardiac pacing and intracardiac ECG recording. One device incorporates fi ve outer surface electrodes to allow bipolar atrial, ventricular, or atrioven-tricular sequential pacing. Although successful pacing is usually achieved intraoperatively in anesthetized patients,175 these catheters are less reliable in intensive care patients owing to the instability of the catheter-endocardial contact. Other PACs have lumina to accept dedicated ventricular or atrial pacing wires and appear to produce a more secure method of temporary pacing.176 In a prospective study of 600 cardiac surgical patients, only 18% of those receiving a pacing PAC required the pacing capability. Predictors of the need for pacing included sinus node dysfunction/bradydys-rhythmias, history of transient complete heart block, aortic stenosis, aortic regurgitation, and cardiac reoperation.177

Right Ventricular Ejection Fraction Pulmonary Artery Catheters

Another modifi cation of the PAC allows measurement of right ventricular ejection fraction (RVEF) using a rapid-response thermistor that measures beat-to-beat changes in PA blood temperature.178 An average residual fraction (RF) of thermal signal with each heart beat can be determined from which ejection fraction (EF) can be calculated.

Because the temperature changes are small, accurate measurement of RVEF depends on two factors: adequate mixing of the thermal bolus and maintenance of a regular heart rate. Although monitoring of RVEF per se may have limited value, other derived variables may be more useful clinically. These include stroke volume, right ventricular end-diastolic volume (RVEDV), and right ventricular end-systolic volume. Right ventricular ejection fraction catheters can aid in the management of right ventricular dysfunction by providing a measure of RVEDV in addition to the tradi-



tional pressure surrogates for ventricular preload, CVP and PAOP. Some evidence suggests that RVEDV is a better index of fl uid responsiveness compared to the PAOP.179 Although its effi cacy remains unproven, the RVEF-PAC might aid management of patients with pulmonary hypertension, right ventricular infarction, right coronary disease, and other con-ditions (e.g., sepsis, ARDS) that require high levels of mechanical ventilation that confound interpretation of cardiac fi lling pressures.180

Mixed Venous Oxygen Saturation Measurement

Mixed venous oxygen saturation measurement provides a method to assess the adequacy of oxygen supply relative to prevailing metabolic demands.181 Assuming the contribution of dissolved oxygen is negligible, rearrangement of the Fick equation reveals the determinants of mixed venous oxygen saturation:

S O S OVO

CO Hbv a2 2

2

1 34100= −

⋅ ⋅⎛⎝⎜

⎞⎠⎟

×�

.

where SvO2 = mixed venous oxygen saturation (%) SaO2 = arterial oxygen saturation (%) V̇O2 = oxygen consumption (mL O2/min) Hb = hemoglobin concentration (g/mL) CO = cardiac output (mL/min) (1.34 mL of oxygen is carried by each gram of

hemoglobin)

Mixed venous oxygen saturation thus depends on four factors: (1) hemoglobin concentration, (2) arterial oxygen saturation, (3) CO, and (4) oxygen consumption. To the extent that arterial hemoglobin concentration, arterial saturation, and oxygen consumption remain stable, mixed venous oxygen saturation refl ects changes in CO, although the rela-tionship is linear only with low baseline CO, becoming cur-vilinear as CO increases.182 In a sense, mixed venous oxygen saturation may be considered the most important index for judging the adequacy of a patient’s hemodynamic status and determining whether the measured cardiac output is suffi -cient, in the context of the patient’s oxygen delivery requirements.183

Special PACs modifi ed with fi beroptic bundles can measure mixed venous saturation continuously based on the differential absorption of various wavelengths of light by oxyhemoglobin and deoxyhemoglobin. The use of multiple wavelengths of light reduces artifact from vessel wall, refl ec-tion from a catheter thrombus, and circulating optically active compounds, such as methylene blue, carboxyhemoglo-bin, or bilirubin. These catheters may show a drift artifact, requiring recalibration in vivo every 24 hours with a PA blood sample. Combined with thermodilution CO measure-ment, mixed venous saturation monitoring allows calcula-tion of other parameters, such as oxygen consumption and delivery. Mixed venous oximetry is safe, convenient, and reliable and gives clinically useful information about the balance between oxygen supply and demand. Studies in the setting of cardiac surgery have demonstrated its usefulness as a continuous monitor to detect changes in CO.184 Two studies showed the benefi ts of using venous oxygen satura-tion to guide goal-directed therapy,145,146 although an older study did not show a benefi t to this monitoring approach.148

Cardiac Output Monitoring

Cardiac output is the total blood fl ow generated by the heart each minute, and at rest ranges from 4.0 to 6.5 L per minute in the normal adult. Preload, afterload, heart rate, and cardiac contractility determine CO, which is regulated to meet tissue metabolic requirements. As such, CO measurement assesses the status of the circulation as a whole and, when combined with other hemodynamic values, additional derived variables, such as pulmonary and systemic vascular resistances, can be calculated.

Thermodilution Cardiac Output

Thermodilution CO (TDCO) measurement is based on the indicator dilution method, in which a known amount of substance is injected into the circulation and its concentra-tion measured over time at a downstream site. For measuring TDCO, a thermistor incorporated into the PAC tip enables continuous measurement of blood temperature in the PA. A second thermistor located at the injectate port measures injectate temperature. When a fi xed volume of cold injectate is used, the temperature drop measured in the PA is used by the computer to calculate CO based on a modifi ed Stewart-Hamilton equation:

COV

=−( ) ⋅

( )∞

∫T T K

T t dt

B I

BΔ0

where V = injectate volume TB = blood temperature TI = injectate temperature K = computation constant

ΔT t dtB ( )∞

∫0

= integral of temperature change over time

The computation constant (K) adjusts for the specifi c heat capacity and specifi c gravity of the injectate and blood, volume of injectate, and size and composition of the PAC.

In clinical practice, the results from two or three con-secutive measurements, performed in rapid succession and varying no more than 10%, is usually averaged to determine the CO. The real-time display of the thermodilution curve helps to identify spurious measurements. Although there is reasonable agreement between thermodilution and other methods of CO measurement, the reproducibility of the TDCO technique is not high.185,186 Therefore, at least a 15% change in CO between two time points is required to signify a clinically signifi cant change.186 Technical errors are common and may go unrecognized.187 Right-sided valvular regurgitation, especially tricuspid regurgitation,188 and intra-cardiac shunts invalidate this method by causing recircula-tion of the thermal bolus and differences between left and right ventricular output. If the injectate port is within the PAC introducer sheath, the thermal bolus is not properly delivered to the RA, producing an abnormal thermodilution curve. Concurrent fl uid boluses through peripheral or central venous catheters introduce additional CO measurement errors, depending on the rate, temperature and timing of the fl uid administered.189


2 532 c h a p t e r 119

The signifi cance of timing TDCO measurements during the respiratory cycle is controversial, owing to the associated changes in RV loading and resulting stroke volume, as well as baseline variation in PA blood temperature.190 Although synchronizing CO measurement at end-inspiration or end-expiration will produce less variation and more reproduc-ibility, a more truly representative mean value for CO is obtained by averaging multiple measurements performed throughout the respiratory cycle. This is especially true when large intrathoracic pressure variations occur, for instance, with positive pressure ventilation.191

A rapid baseline drift in pulmonary artery blood tempera-ture has been described early after discontinuation of hypothermic cardiopulmonary bypass. This may cause underestimation of the true CO in the fi rst 10 to 15 minutes after bypass.192 Although use of ice-cold injectate was sug-gested to produce more accurate results than room tempera-ture injectate by increasing the signal-to-noise ratio of the thermal bolus, several investigators have shown no practical difference in accuracy between the two methods.193,194 Con-versely, some data suggest that ice-cold injectate may cause transient decreases in heart rate and cardiac output.195 Con-sequently, the simpler method applied in most clinical set-tings employs a 10-mL room temperature injectate. The thermodilution technique is simple to perform repeatedly and quickly, requires only basic clinical skills, obviates the need for repeated blood sampling, and uses a nontoxic, non-recirculating, and nonaccumulating indicator. For these reasons, TDCO is extensively utilized as the preferred method in a variety of clinical settings.

Transpulmonary Thermodilution Cardiac Output Measurement

One of the main disadvantages of the traditional TDCO technique is the requirement for PA catheterization, with its attendant risks. Also, the PAC cannot be used in very small children. Newer devices employ a special thermistor-tipped arterial catheter that can measure blood temperature changes in the systemic circulation (either femoral or axillary artery) following bolus administration of ice-cold injectate delivered through a central venous line.196 As the measurement is made over a longer period of time than standard TDCO measurements, the infl uence of the respiratory cycle on CO variation is eliminated. In patients after cardiac surgery, a good correlation was found between transpulmonary ther-modilution CO and conventional TDCO, although the trans-pulmonary values tended to be higher, possibly refl ecting loss of heat during transfer through the lungs.197 The trans-pulmonary thermodilution technique has the added advan-tage of derived variables refl ecting extravascular lung water and intrathoracic blood volume, a measure of preload.198

Lithium Dilution Cardiac Output Measurement

Indicator dilution measurement of cardiac output can be achieved using ionized lithium as an indicator. Lithium chloride is given as a bolus via venous catheter, and the dilu-tion curve is measured by a lithium-sensitive electrode, over which arterial blood from a regular arterial catheter is drawn at a constant rate during each measurement.199,200 Small

boluses of lithium (0.15–0.3 mmol) allow as many as fi ve to ten measurements per day. Studies indicate that accuracy is high and respiratory infl uences are obviated because CO is measured over several respiratory cycles. The injection of the lithium indicator can be done through a peripheral vein without sacrifi cing accuracy, so that the measurement does not even require insertion of a central line.201 In very small children, lithium dilution CO has been shown to be compa-rable to transpulmonary thermodilution CO.202 One possible drawback of the method for intraoperative use is potential interference by several neuromuscular blocking agents with the ion-selective lithium electrode.

Continuous Thermodilution Cardiac Output Measurement

As heat is the only nonaccumulating indicator, continuous CO measurement methods have focused on modifi ed ther-modilution techniques. One method introduces the thermal signal through a PAC that has a blood warming fi lament in the RV located 14 to 25 cm from the catheter tip. Thermal damage does not occur because of the brief duration of contact between heating fi lament and the blood and myocar-dium, as well as control of fi lament temperature below 44°C. Continuous TDCO measurement uses a small thermal signal that is detectable above the background thermal noise. Computer-controlled algorithms utilizing a stochastic system control fi lament switching between on and off states in a random process, with auto–cross-correlation to mini-mize temperature peaks and enhance signal to noise ratio.203 The displayed CO is updated every 30 seconds and represents an average CO measured over the previous 3 to 6 minutes. Although this averaging delays the response time of continu-ous thermodilution CO measurement, confounding respira-tory infl uences are attenuated, yielding a more accurate average cardiac output.

Compared to other methods of CO measurement, con-tinuous thermodilution CO measurement is reasonably accurate and precise.204 However, thermal noise contributes a large source of error and is particularly problematic follow-ing hypothermic cardiopulmonary bypass.205 Continuous TDCO measurement should not be considered “real-time” but rather a trend of recent measurements. As such, it is not suitable for identifying acute hemodynamic changes, unlike direct arterial blood pressure monitoring or mixed venous oxygen saturation. However, compared to bolus CO measure-ment performed intermittently every several hours, the con-tinuous CO method provides information earlier and may allow more timely clinical intervention.204 As the system is fully automated, it requires less procedural effort than bolus TDCO methods and may decrease the risks of fl uid overload, infection, and measurement error.

Esophageal Doppler Cardiac Output Measurement

The Doppler principle uses the spectral frequency shift of ultrasound waves refl ected from a moving target to calculate the velocity of the target. Doppler-based CO measurement employs high frequency (2–5 MHz) ultrasound refl ected from circulating red blood cells, as described by the Doppler equation:



Vf c

f=

⋅⋅2 0 cosθ

where V = velocity of blood f = frequency shift f0 = transmitted ultrasound frequency θ = angle between the ultrasound beam vector and

velocity vector c = velocity of ultrasound in blood (approximately

1540 m/sec)If the angle of insonation is within 20 degrees of blood

fl ow direction, the error in velocity measurement is less than 6%, because cosine 20 degrees = 0.94.

A Doppler probe positioned in the suprasternal notch allows insonation of the ascending aorta and is a noninvasive and accurate method to measure aortic blood fl ow, but it is labor intensive and requires considerable operator expertise. Signal acquisition cannot be obtained in some patients with short necks, emphysema, or aortic valve disease, and since the probe cannot be fi xed in position, this method cannot be used for continuous CO monitoring. As an alternative, the esophagus offers a suitable site for probe placement for con-tinuous Doppler CO monitoring.206 A probe of similar dimen-sions to an orogastric tube is inserted into the lower esophagus, approximately 35 to 40 cm from the incisor teeth. From this imaging position, the thoracic aorta and esophagus lie parallel to one another, thereby providing a suitable acoustic window to obtain a reliable Doppler signal from the descending aorta. With a short period of training, repro-ducible Doppler measurements are technically easy to acquire in less than 5 minutes.207,208 However, the esophageal Doppler technique has generally been limited to tracheally intubated patients. There are no reports of complications arising from esophageal Doppler monitoring, but theoreti-cally, one might expect complications similar to those seen during intraoperative TEE (vide infra); special care should be taken when esophageal pathology exists or when the patient is anticoagulated.

Rather than an actual measurement of cardiac output, Doppler CO monitors provide an estimate of stroke volume from the aortic blood fl ow velocity-time integral. The mea-sured values can either be reported as descending aortic blood fl ow, or multiplied by a constant (∼1.4) to give esti-mated total body cardiac output. Additional indices derived from the aortic blood fl ow and the shape of the velocity-time envelope provide information on preload, afterload, and con-tractility (Fig. 119.13). Stroke volume estimation is based on the following assumptions: (1) The angle of insonation of blood fl ow remains constant. (2) The fraction of CO passing through the descending thoracic aorta remains constant despite changes in total CO, preload, afterload, and tempera-ture. (3) The descending thoracic aorta cross-sectional area does not change during systole. (4) Diastolic fl ow in the descending aorta is negligible. In view of these assumptions, it is not surprising that esophageal Doppler CO measure-ments tend to underestimate CO measured by other methods, although they accurately track changes occurring over time.209–212 Some improvement in accuracy may be achieved by devices incorporating an M-mode transducer into the probe, enabling continuous measurement of the aortic diam-eter rather than using a nomogram to calculate the aortic

cross-sectional area.210 Despite these theoretical limitations of this technology, using Doppler-based CO to monitor trends in CO has proven clinically effective for resuscitating criti-cally ill and surgical patients. In both cardiac and noncardiac surgery, intraoperative esophageal Doppler-guided fl uid therapy has been shown to reduce complications and to shorten hospital length of stay.149,151,213

To recap, the esophageal Doppler monitor is safe to use and provides unique information on the state of the circula-tion. It remains to be seen if large studies will demonstrate effi cacy and cost-effectiveness and ensure a place for this technique as a routine cardiovascular monitor.

Pulse Contour Cardiac Output

Pulse contour methods derive the CO from the arterial pres-sure waveform. Available commercial devices rely on differ-ent models of the circulation, but all need to be calibrated against a known CO prior to monitoring in order to refi ne the parameters used in the CO calculations (e.g., vascular resistance, compliance, impedance, wave refl ectance).214 Recalibration is usually recommended every 4 to 8 hours. Reliable measurements require the presence of a reasonably defi ned arterial waveform and absence of frequent arrhyth-mias. However, one study has shown preserved accuracy of CO monitoring despite a wide range of dynamic response characteristics of the arterial blood pressure monitoring system.215 Marked changes in systemic vascular resistance affect the refl ection of the pulse wave from the peripheral blood vessels and may require monitor recalibration to avoid reduced accuracy of the pulse contour CO measurements.215,216 Despite some limitations, pulse contour methods do provide a true continuous beat-to-beat minimally invasive measure-ment of CO. Several studies have shown clinically acceptable agreement between pulse contour CO and TDCO.217–219

Preload reduction

Positive inotropy

Myocardial depression

Predominant change

Preload increase

Afterload increase

Afterload reduction

Mean acclerationVelocity

Velocity

Flow time Time

Peak

FIGURE 119.13. Spectral Doppler of velocity waveforms recorded using esophageal Doppler cardiac output monitoring. Changes in waveform shape result from alterations in inotropic state, preload, and afterload. The Doppler waveform pattern changes in a consis-tent manner: inotropic changes affect peak velocity and mean accel-eration, preload changes affect systolic fl ow time corrected for heart rate (FTc), and afterload changes affect FTc and peak velocity.


2 53 4 c h a p t e r 119

Additionally, pulse contour methods can measure the varia-tion in stroke volume induced by positive pressure ventila-tion. Just as the respiratory variation in systolic blood pressure may be used to refl ect volume status and predict CO response to fl uid challenge, measurement of stroke volume variation may be equally useful as a monitor of the adequacy of cardiac preload. While some clinical investigations have demonstrated the utility of stroke volume variation monitor-ing,220–222 others have not.223

Intraoperative Transesophageal Echocardiography

Intraoperative monitoring with cardiac ultrasound was fi rst described in 1980 using M-mode transesophageal echocar-diography (TEE),224 but expanded rapidly with the advent of two-dimensional sector scanning225 and the introduction of smaller phased array transducers.226 Early intraoperative studies focused predominantly on monitoring global left ven-tricular function and detecting segmental wall motion abnormalities (SWMAs) indicative of myocardial ischemia. Technological developments, including biplane and subse-quently, multiplane transducers, color fl ow imaging, and other Doppler modalities, have provided a plethora of struc-tural and hemodynamic information stimulating dramatic increases in utilization of intraoperative TEE. At the current time, it is the only method that provides instantaneous, continuous, dynamic, real-time hemodynamic information that can be used intraoperatively to diagnose and monitor critical cardiac abnormalities or changes in function.

However, the increasing complexity of both the equipment and the data now available, the specifi c demands of the intra-operative environment, as well as the blurring of the distinc-tion between TEE as a “monitor” and “diagnostic modality” have combined to present new responsibilities and chal-lenges to the clinician using this technology in the operating room.227

Indications

Cardiac Surgery

The use of TEE in cardiac surgery has become routine in many centers, although the evidence for this practice in all cases is debatable. Specifi c guidelines published by the Amer-ican Society of Anesthesiologists/Society of Cardiovascular Anesthesia Task Force on Transesophageal Echocardiography (ASA/SCA) remain unchanged from those formulated in 1996 (Table 119.6), with indications separated into three categories depending on the strength of evidence supporting the use of TEE in specifi c clinical scenarios.174 Despite its classifi cation as category II for use in routine coronary artery bypass surgery (CABG), TEE in high-risk patients seems to be associated with better operative outcome.228,229 In addition, a variety of reports have documented the utility of TEE monitoring both before and after cardiopulmonary bypass. In a series of more than 5000 patients, Mishra et al.230 reported that the pre-bypass study identifi ed unsuspected fi ndings in 22.9% of patients. These fi ndings led to minor changes in surgical technique in 18% and major changes in 4.9% of cases. The post-bypass TEE proved especially useful for guiding surgical

TABLE 119.6. Indications for transesophageal echocardiography (TEE) during cardiac surgery

Cardiac surgical procedure Evidence TEE assessment

Coronary artery bypass grafting Category II Wall motion/thickening abnormalities Contrast echocardiographyValve repair Category I Extent/mechanism of disease Post-bypass valvular function Intracardiac airValve replacement Category II Prosthetic valvular function post-bypass Paravalvular leak Intracardiac airThoracic aorta Category II Presence/severity for atherosclerosis (site of aortic cross-clamp and possible

modifi cation of cardiopulmonary bypass) Category I/II Aortic dissection and its complicationsCongenital heart disease Category I Confi rmation of known abnormalities Diagnosis of unsuspected abnormalities Adequacy of repair Intracardiac airPlacement of monitoring and Category III Pulmonary artery catheter therapeutic devices Intraaortic balloon pump Coronary sinus catheter, venous drainage cannula Endoaortic balloon clamp in minimally invasive surgeryMiscellaneous Category I Myectomy (hypertrophic obstructive cardiomyopathy) Transmyocardial laser revascularization

Indications for TEE as described in the American Society of Anesthesiologists/Society of Cardiovascular Anesthesia—ASA Practice Guidelines for Periopera-tive Transesophageal Echocardiography. Category I: Supported by the strongest evidence or expert opinion; TEE is frequently useful in improving clinical out-comes in these settings and is often indicated, depending on individual circumstances. Category II: Supported by weaker evidence and expert consensus; TEE may be useful in improving clinical outcomes in these settings, depending on individual circumstances, but appropriate indications are less certain. Category III: Little scientifi c or expert support; TEE is infrequently useful in improving clinical outcomes in these settings, and appropriate indications are uncertain.



efforts to remove intracardiac air collections. Overall, 38.8% of patients were felt to have benefi ted from the pre-bypass study and 39.2% from the post-bypass study.230 Click et al.231 also found new information in 15% of pre-bypass and 6% of post-bypass studies in a review of 3245 cardiac surgery patients. These fi ndings directly affected surgical decision making in 14% of cases.

Transesophageal echocardiography is felt to be particu-larly useful for valvular procedures.232,233 It is invaluable for mitral valve repair and reconstruction, with 92% agreement on mechanism and location of pathology between TEE diag-noses and surgical fi ndings.234 The accuracy of TEE in iden-tifying defective leafl et segments has been reported at 90% to 97%, being best for the middle scallop of both the anterior and posterior leafl ets.235 However, several investigators have reported the tendency of intraoperative TEE to underesti-mate the severity of MR when compared to angiography or preoperative transthoracic echocardiography (TTE).236,237 This is especially important to keep in mind when consider-ing changes to the surgical plan based on the intraoperative TEE performed immediately prior to bypass.

Shapira et al.238 also found TEE most frequently helpful in decisions concerning whether to replace or repair the mitral valve, followed in frequency by those concerning the tricuspid valve. In this series, therapeutic decisions were affected by the prepump TEE in 29.3% of cases, while the postpump study led to immediate return to bypass for surgi-cal correction of technical errors in 3.6% of cases.238 Follow-ing valve replacement or repair, TEE is especially useful for evaluating paravalvular leaks, leafl et motion, and other forms of valvular dysfunction (Fig. 119.14). In addition, onset of new SWMA may indicate coronary ostial obstruction fol-lowing aortic valve surgery and allow immediate return to bypass for required surgical revision.

Another important intraoperative application of TEE is the examination of those portions of the aorta to be manipu-lated during cardiac surgery. Both TEE and high-frequency epiaortic probes have been used successfully for this purpose. The incidence of neurocognitive dysfunction following cardiac surgery ranges between 20% and 80% depending on the defi nition and evaluation method and is felt to be related to atherosclerotic disease of the ascending aorta and the trauma it undergoes during heart surgery.239 Extensive disease seen in the region planned for placement of the aortic bypass cannula or cross-clamp or the proximal coronary graft anastomoses may lead to alternative surgical manage-ment strategies. These include use of various aortic fi ltration or defl ection devices, jump-grafting off an internal mammary graft rather than the ascending aorta, cannulation of an alter-native arterial site (femoral or axillary vessel), or even surgi-cal replacement of a highly diseased ascending aorta. In addition, there is evidence that the risk of perioperative stroke can be lowered by tailoring procedures based on the degree of atherosclerotic disease seen by TEE in the aortic arch during routine CABG surgery.240

Surgical correction of congenital heart disease is a cate-gory I indication for intraoperative TEE. Several large obser-vational studies have documented the crucial role of the pre-bypass study in defi ning anatomy, as well as the post-bypass study in assessing adequacy of the repair.241,242 Cur-rently available TEE probes (with tip diameter as small as 7.5 mm) can be used safely in children as small as 2 kg. Bettex

A

BFIGURE 119.14. (A) Mid-esophageal, fi ve-chamber, color Doppler view demonstrating a moderate paravalvular regurgitant leak fol-lowing bioprosthetic aortic valve replacement. This defect may be due to technical error or an intrinsic defect in the prosthesis. (B). Mid-esophageal, four-chamber, color Doppler view of a mitral mechanical prosthesis showing dehiscence of the sewing ring from the mitral annulus necessitating return to cardiopulmonary bypass for immediate surgical revision.

et al.243 reported TEE to be “essential” to intraoperative hemodynamic management in almost 20% of cases, most often for adjustment of preload, and “infl uential” in surgical decision making in 13.1%. Another group reported TEE to be “decisive” in management of 8% of their patients, almost half of which required a second bypass run.244

Over the past decade, TEE use during cardiac surgery has increased, and in the eyes of some has even supplanted the role of other invasive monitors in guiding intraoperative hemodynamic monitoring.230,245 There is some compelling evidence suggesting that intraoperative TEE improves outcome in a cost-effective manner.246 In 2003, the American College of Cardiology/American Heart Association/Ameri-can Society of Echocardiography Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiog-raphy published new guidelines that included a section that addressed intraoperative echocardiography (Table 119.7). These new guidelines were based on the original ASA/SCA guidelines, as well as an additional 118 peer-reviewed journal articles that have been published since 1996. These guide-


2 53 6 c h a p t e r 119

lines refl ect new technologies and developments as well as changes in practice that have occurred in the past decade. The only remaining class III indication for intraoperative TEE is surgical repair of an uncomplicated secundum atrial septal defect, with class III evidence defi ned as “not useful/effective and in some cases . . . even harmful.”247 Class II indications are divided into two groups to further differenti-ate between those indications for which evidence is generally good (IIa), and those for which evidence is still controversial (IIb). Of note is the dramatic increase in the number of cate-gory I indications. Other technologies, such as contrast or three-dimensional echocardiography, may also increase the utility of TEE in the operating room by further assisting the surgeon in customizing each procedure and optimizing the patient’s condition prior to its completion, and may fi nd their way onto these indication lists in the future.

Noncardiac Surgery

Use of TEE has been traditionally the purview of the cardiac division of most anesthesia departments, and this is refl ected

in the guidelines listed in Table 119.8. The only category I indication for TEE use in noncardiac surgery is for diagnosis of severe intraoperative hemodynamic instability. There is no question of its value in confi rming or excluding certain cardiac and noncardiac diagnoses in the unstable patient. Brandt et al.248 reported 66 cases in which TEE was used to successfully determine the etiology of hemodynamic collapse, the most common of these being left ventricular dysfunction, new regional wall motion abnormalities, and aortic dissection.

Use of TEE in patients with category II indications has been increasing as familiarity with the technology has increased. Those with category II indications are defi ned as “patients at increased risk of myocardial ischemia or hemo-dynamic disturbance.”249 In a database review of 99 patients with category II indications in whom TEE was used as an intraoperative monitor, 165 new fi ndings were recorded, of which changes in right and left ventricular systolic function were the most common. Transesophageal echocardiography was most infl uential in those patients with known pulmo-

TABLE 119.7. Indications for intraoperative echocardiography, updated 2003, American College of Cardiology, American Heart Association247

Category I (general agreement that TEE is useful/effective) Evaluation of acute, life-threatening hemodynamic instability Valve repair Aortic dissection +/− aortic replacement Myectomy Complex valve replacements +/− homografts or coronary

reimplantation Congenital repairs requiring cardiopulmonary bypass Placement of intracardiac devices (i.e., port-access procedures) Evaluation of posterior or loculated pericardial window

procedures Intraoperative evaluation of endocarditis when preoperative

testing was inadequateCategory IIa (opinion is in favor of usefulness/effi cacy but controversy persists) Surgical procedures in patients at increased risk for cardiac

morbidity or hemodynamic instability Evaluation of valve replacement/repair Evaluation of aortic atheroma burden Maze procedure Cardiac tumors Pulmonary embolectomy, thrombectomy Cardiac aneurysm repair Evaluation for intracardiac air during cardiotomy, heart

transplants, sitting neurosurgical proceduresCategory IIb (usefulness/effi cacy is less well established by evidence or opinion) Evaluation of suspected cardiac trauma Dobutamine stress echocardiography Evaluation of myocardial perfusion, coronary anatomy or graft

patency Pericardial effusions, pericardiectomy Assessment of residual fl ow after patent ductus arteriosus

closure Evaluation of regional wall motion during and after off-pump

procedures Evaluation of thoracic aortic repair proceduresCategory III (evidence or agreement that TEE is not useful/ effective and may be harmful) Surgical repair of uncomplicated secundum atrial septal defect

TABLE 119.8. Indications for transesophageal echocardiography (TEE) during noncardiac surgery

Preexistingcardiac disease Evidence TEE assessment

Coronary artery Category II Global LV function disease Segmental wall motion and

thickening Functional mitral regurgitationCardiomyopathy Category II Ventricular size and function Functional valvular

regurgitation (MR, TR) LVOT velocity, SAM, and MR

(HCM)Valvular disease Category II Severity of regurgitation Impact of loading changes upon

valvular regurgitation or stenosis

Impact of loading changes on ventricular function

Miscellaneous Category I Diagnosis of severe intraoperative hemodynamic

instability Category III Troubleshooting/confi rmation

of intracardiac catheters, etc. Category III Monitoring for embolization of

air, thrombus, bone marrow Paradoxical embolization

Indications for TEE as described in the American Society of Anesthesiolo-gists/Society of Cardiovascular Anesthesia—ASA Practice Guidelines for Perioperative Transesophageal Echocardiography. Category I: Supported by the strongest evidence or expert opinion; TEE is frequently useful in improv-ing clinical outcomes in these settings and is often indicated, depending on individual circumstances. Category II: Supported by weaker evidence and expert consensus; TEE may be useful in improving clinical outcomes in these settings, depending on individual circumstances, but appropriate indications are less certain. Category III: Little scientifi c or expert support; TEE is infre-quently useful in improving clinical outcomes in these settings, and appro-priate indications are uncertain; LV, left ventricle; MR, mitral regurgitation; TR, tricuspid regurgitation; LVOT, left ventricular outfl ow tract; SAM, sys-tolic anterior motion; HCM hypertrophic cardiomyopathy.



nary arterial hypertension and right heart failure, and in those undergoing lung or liver transplantation.249 Denault et al.250 showed that even in category II and III patients, TEE altered therapy in 31% and 21% of cases, respectively. Suriani et al.251 showed that in a series of 123 liver transplant recipi-ents, TEE had a major impact (defi ned as treatment of a potentially life-threatening event) in 15% of patients, while 81% of patients had their care altered in some way by their TEE evaluation.

The development of endovascular repair procedures involving the descending thoracic aorta has given TEE a new role as an adjunct to fl uoroscopy in the operating room. It has been shown to be safe and effective in defi ning the extent of the aneurysm sac, useful for choosing an appropriate “landing zone” for the prosthesis, and valuable for identify-ing the intimal tear. It is unique in its ability to differentiate the true lumen from the false lumen and to confi rm the presence of the surgical guidewire in the true lumen. Finally, TEE compares favorably with angiography in its ability to evaluate “endoleaks” (sites of graft leakage) after device deployment, at times identifying leaks missed by conven-tional angiography.252–255

Transesophageal echocardiography has also been shown to be useful in a variety of other operative settings. Among these is liver transplantation, specifi cally in the manage-ment of the intense hemodynamic instability that can accompany graft reperfusion.249,256 It is also helpful in guiding vasodilator use and evaluating the adequacy of vascular anas-tomoses during lung transplantation.249,257,258

Contraindications

Contraindications to intraoperative TEE monitoring are the same as those for awake patients. These include oropharyn-geal, esophageal, and gastric pathology, particularly obstruc-tive and hemorrhagic lesions. In addition, the presence of unstable cervical spine injuries, facial trauma, a history of mediastinal radiation, or severe coagulopathy necessitates consideration of the risks and benefi ts for each individual patient. The site of surgery may preclude use of TEE, for example, during surgery on the upper gastrointestinal tract or airway. Other conditions in which the risk of TEE may be increased include severe esophageal refl ux disease, severe odynophagia, and dysphagia. In addition, surgical position-ing may severely impede TEE monitoring or prohibit probe manipulation during surgery. For instance, extreme neck fl exion during neurosurgical procedures performed in the sitting position has been associated with postoperative vocal cord paralysis in patients in whom intraoperative TEE moni-toring was used to detect venous air embolism.259

Probe Insertion

Placement of the TEE probe for intraoperative monitoring occurs after induction of general anesthesia and endotracheal intubation. The lubricated probe tip is placed behind the endotracheal tube with the mandible lifted upward by a gloved hand to open the pharynx, a maneuver known as the Esmarch maneuver.260 This allows the probe tip, with the wheels unlocked, to be guided easily into the mouth, pharynx, and esophagus, to an approximate depth of 15 to 20 cm from

the incisors. A few individuals require direct laryngoscopy for probe placement. Under no circumstances should the probe be advanced against resistance, as manipulation in the presence of unsuspected pathology may result in severe injury. Failure of probe placement is uncommon. In a series of 901 patients, a failure rate of only 1.2% was reported.261

Intraoperative Ischemia

Since the early 1980s, perioperative myocardial ischemia has been identifi ed repeatedly as a risk factor for adverse post-operative outcome. This association has driven efforts to im -prove intraoperative monitoring for ischemia and therapies based on its detection. In initial investigations, TEE monitor-ing of global and segmental left ventricular function appeared to be the ideal modality for early detection of intraoperative ischemia.262 These early clinical reports were consistent with experimental evidence showing that acute coronary occlu-sion produced echocardiographically detectable SWMAs before characteristic ECG changes appeared.263,264

However, both conceptual and practical problems limit TEE as an intraoperative ischemia monitor. Although SWMAs reproducibly occur before ECG changes when ischemia is produced by balloon occlusion of a coronary artery, acute coronary occlusion may not be the appropriate mechanism for modeling most intraoperative ischemic events. Also, factors other than myocardial ischemia may be responsible for intraoperative SWMAs. These include conduction abnor-malities (left bundle branch block, ventricular pacing), as well as abrupt changes in left ventricular preload and afterload as occurs following aortic cross-clamping during thoracic or abdominal aortic surgery. Marked increases in right ventricu-lar preload or afterload may cause septal motion abnormali-ties that may be misinterpreted as ischemic changes. Even slight rotation or translation of the heart can appear as SWMAs when in fact none has occurred. Myocardial stun-ning can also cause changes in wall motion in the absence of ischemia. Furthermore, intraoperative SWMAs often occur in the absence of hemodynamic changes, making it diffi cult to determine optimal treatment for these TEE changes.265,266 For example, during abdominal aortic surgery, transient SWMAs do not appear to have any immediate postoperative signifi cance.267 Use of intraoperative TEE to monitor for isch-emia is confounded further by the fact that no gold standard exists to validate the TEE fi ndings. Although TEE has been reported to be more predictive than ECG in identifying patients who suffer perioperative infarction, concordance between TEE and ECG-detected ischemia is poor.266,268,269

Beyond these conceptual limitations are the practical diffi culties of TEE monitoring for intraoperative ischemia. Probe positioning must be stable in order to detect SWMAs properly. Interpretation of new SWMAs most be placed in the appropriate clinical context that includes the surgical proce-dure, changes in ventricular loading conditions, conduction abnormalities, and data provided by other physiologic vari-ables (ECG, blood pressure, CVP, PAP, and so on). Like most methods of hemodynamic “monitoring,” TEE is only as con-tinuous as the intermittent attention span of the anesthesi-ologist, an individual who is continuously scanning a variety of monitors and situations, not least of which is the surgical fi eld.


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A variety of innovations have been proposed to improve the usefulness and accuracy of TEE as a monitor of myocar-dial ischemia. Technical advances in echocardiography, such as “automated border detection” have tried to make TEE monitoring more continuous and recordable, but these methods require frequent adjustment of gain settings and are disturbed by even slight probe movement.270 Echocardio-graphic contrast agents can identify blood fl ow in the myo-cardium, although their use has not become widespread. Use of dobutamine stress testing has gained some ground in dif-ferentiating infarcted from stunned myocardium in the acute setting. A trial of low-dose dobutamine may improve the function of stunned myocardium while it has no effect or may have a deleterious effect on infarcted or ischemic tissue.271 Other technologies, including color kinesis and myocardial tissue Doppler imaging, may prove useful for ischemia detection but remain limited in their application at present.272,273 However, while routine TEE monitoring for ischemia is limited by the above-mentioned considerations, it may prove extremely valuable in evaluating complex and dynamic clinical dilemmas, including the diagnosis of myo-cardial ischemia in the hemodynamically unstable patient.

Complications

Complications of TEE are the result of mechanical trauma to the upper gastrointestinal tract and oropharynx, and include abrasion, laceration, and perforation. The conse-quences of TEE probe-induced trauma range from minor postoperative pharyngeal discomfort to major gastric or esophageal injury274 leading to hemorrhagic shock, medias-tinitis, or peritonitis.275–277 While intraoperative TEE may

slightly increase these risks as clinicians may attempt more vigorous probe insertion or manipulation in anesthetized patients, there are no data to support this assertion. Intraop-erative TEE is frequently performed in patients who are at increased risk for complications, owing to intraoperative hypothermia and profound anticoagulation for cardiopulmo-nary bypass, yet severe complications appear to be rare events. A single-center review of 7200 cardiac cases moni-tored with intraoperative TEE showed a morbidity rate of 0.2% and a mortality rate of 0%. Three major events reported, included a single esophageal perforation and two upper gas-trointestinal hemorrhages, both detected on placement of an orogastric tube at the conclusion of the procedure.278 Even in children, use of TEE seems very safe. In a series of 532 cases, complications included only one unintentional tracheal extubation (without sequelae). There was one case of tracheal or bronchial compression that resolved on removal of the probe, and nine cases of blood-tinged probe noted on removal, but with no patient morbidity.244 Other reported complica-tions of TEE include bacteremia279,280 and postoperative esophageal dysmotility.281

Discussion

Given the rich diagnostic information provided by TEE, the clinician utilizing this monitor in the operating room has a tool that gives unique information that exceeds and differs from that of traditional intraoperative monitors. Virtually all the routinely measured hemodynamic variables (CVP, PAP, etc.) may be estimated using TEE, albeit with some expertise and considerable effort (Tables 119.9 and 119.10). However, the greatest value of intraoperative TEE is its integration into

TABLE 119.9. Transesophageal echocardiography (TEE) monitoring for assessment of ventricular and valvular function

Two dimensional Color fl ow/Doppler Other

Systolic function Global Fractional area change Automatic border detection Fractional volume change Color kinesis Fractional shortening (M-mode) Segmental Segmental wall motion Tissue Doppler abnormalities Segmental wall thickening abnormalitiesDiastolic function General End-diastolic area/volume Mitral valve fl ow (E : A ratio, E Isovolumic relaxation time deceleration time and slope) Color M-mode Pulmonary venous fl ow Negative dP/dt (mitral regurgitation) Pericardial disease Pericardial constriction, Respiratory variation in effusion, or localized transvalvular fl ow compression velocity Chamber size Early diastolic RV collapse Late systolic RA collapseValvular function Regurgitation Structural abnormalities Regurgitant jet length, width, area PISA Pulmonary venous (MR) and hepatic Regurgitant jet velocity venous (TR) systolic infl ow blunting Pressure half time (AI) or reversal Stenosis Structural abnormalities Increased color velocity and variance Continuity equation valve area Valve planimetry peak and mean valve gradients

RV, right ventricle; RA, right atrium; PISA, proximal isovelocity surface area; MR, mitral regurgitation; TR, tricuspid regurgitation; AI, aortic incompetence.



the traditional monitoring array for high-risk patients, both cardiac and noncardiac. In this way, intraoperative abnor-malities may be detected and rejected or confi rmed quickly and accurately, further diagnostic workup directed as neces-sary, specifi c diagnoses ruled out or outcomes avoided, treat-ment customized as possible, and ongoing conditions carefully watched. Echocardiography is a rapidly evolving fi eld, with each year bringing new technologies and innova-tions into the hands of the clinician. It is the hope that these will only hone its application and improve its promise.

Summary

In recent decades, technologic advances and increasingly invasive monitoring techniques have dramatically increased the amount and diversity of data available to the physician caring for critically ill patients in the intraoperative setting. This is especially important in the operating room as the induction of general anesthesia itself causes disruption of normal homeostasis and can result in hemodynamic insta-bility in high-risk patients. Early detection and treatment of such cardiovascular changes before irreversible harm occurs is the goal of hemodynamic monitoring. As such, a hierarchy of increasingly invasive monitoring techniques has evolved, each carrying correspondingly increasing risks of complica-tions. A patient’s degree of benefi t and potential risk must be assessed individually. Monitors are designed and intended to augment, not replace, the clinical skills of the physician. Knowledge of the individual patient, clinical judgment and integration into the clinical scenario is crucial for any one of these intraoperative monitors to be used effectively and safely.

Although electrocardiography (ECG) monitoring has been standard for many decades, there is still controversy concerning its utility. There is increasing evidence to support ECG monitoring for myocardial ischemia into the postopera-tive period for high-risk patients. It appears that most ST-segment changes occur in the absence of hemodynamic lability, and that keeping hemodynamic variables within 20% of their baseline values does not appear to reduce intra-

operative ischemic events. Monitoring V5 in addition to one other lead (II, III, V4, or V5) allows 90% sensitivity of ischemia detection.

Invasive measurement of arterial blood pressure is indi-cated for one of a very few reasons: (1) anticipation of large or abrupt hemodynamic changes; (2) coexisting disease that necessitates close hemodynamic management; (3) mechani-cal or pharmacologic intervention is planned or anticipated (for example, placement of an intraaortic balloon counterpul-sation device, or the need for hypotensive anesthesia); or (4) noninvasive methods that are impractical or impossible. Overall, invasive arterial blood pressure monitoring is very safe, with a complication rate near 0.1%. Additional informa-tion can be gleaned from the waveform. For example, exces-sive variation in the systolic blood pressure is often an indicator of hypovolemia, or a very prolonged systolic time can be an indicator of a poor myocardial function.

Central venous pressure refl ects a balance among intra-vascular volume, venous tone, and right ventricular volume. A single, isolated pressure reading provides little useful information unless it is extremely high or low. Portable, hand-held ultrasound devices have made it possible to image the great veins of the neck prior to or during cannulation, increasing success while reducing complication rates.

Confl icting evidence has emerged as to whether PAC monitoring improves outcomes or increases risk of harm. It is possible that the most dangerous aspect of PAC use is misinterpretation of data in the hands of an inexperienced operator. Current recommendations from the American Society of Anesthesiologists specify that PAC use be limited to high-risk patients undergoing high-risk surgery, under practice conditions considered favorable (i.e., knowledgeable and experienced physicians and nurses). However, there are also data that perioperative, goal-directed therapy, such as optimization of oxygen delivery and cardiac index using PAC-derived data, can reduce mortality and morbidity. Use of specialized PACs, providing mixed venous oxygen satura-tion data, might be another end point for further goal-directed therapy studies.

Although the thermodilution method for measuring cardiac output (CO) has been the standard monitor for many

TABLE 119.10. Transesophageal echocardiography (TEE) hemodynamic information

Two dimensional Color fl ow/Doppler

Cardiac output/stroke Fractional ventricular volume LVOT/RVOT velocity time integral volume change multiplied by respective outfl ow tract

diameterLVEDP Aortic regurgitant jet velocity at end

diastole Pulmonary venous fl owLAP Left atrial size Motion of interatrial septumPAP systolic Pulmonary artery size RV Peak TR jet velocity structure and functionPAP diastolic RV structure and function End-diastolic PR jet velocityRAP RA size Vena caval size, changes with respiration

LVEDP, left ventricular end-diastolic pressure; LAP, left atrial pressure; PAP, pulmonary artery pressure; RAP; right atrial pressure; LVOT, left ventricular outfl ow tract; RVOT, right ventricular outfl ow tract; TR, tricuspid regurgita-tion; RV, right ventricle; PR, pulmonic regurgitation; RA, right atrium.


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years, several newer methods have been developed that obviate the need for the PAC. Lithium dilution and transpul-monary arterial thermodilution both appear to have similar accuracy. Pulse-contour methods derive continuous beat-to-beat CO from the arterial pressure waveform and allow mea-surement of stroke volume variation, an index of the adequacy of cardiac preload. Esophageal Doppler CO measures distal aortic blood fl ow with a probe in the distal esophagus.

At the current time, TEE is the only method that pro-vides instantaneous, continuous, dynamic, real-time hemo-dynamic information that can be used intraoperatively to diagnose and monitor critical cardiac abnormalities or changes in function. It has proven especially useful for valve replacement and repair procedures, congenital heart disease surgery, evaluation of the aorta prior to heart surgery, guiding efforts at removing intracardiac air prior to separation from cardiopulmonary bypass, as an adjunct to angiography and fl uoroscopy during endovascular procedures on the thoracic aorta, and in diagnosis and monitoring of hemodynamically unstable patients undergoing noncardiac surgery.

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