Common Pitfalls and Artifacts in Hemodynamic Monitoring

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Objectives:n Review available hemodynamic monitoring

technologies for critically ill childrenn Refresh knowledge of artifacts and technical

limitations inherent in clinical physiologic measurements

n Identify pitfalls in interpretation and application of hemodynamic data in the clinical setting

Key words: hemodynamic monitoring, venous oxygen saturation, lactate, pulmonary artery occlusion pressure, thermodilution, capnography

iNtRODUctiON

Heisenberg’s uncertainty principle, which was proposed in the early days of atomic and subatomic particle physics research, has applicability in pediatric critical care hemodynamics. In essence, the very act of measuring a physiologic variable may affect the value of that variable. It is therefore appropriate to approach the discussion and the use in practice, of imperfect measures of the status of our patients with humility and with constant vigilance for potentially misleading information.

Pediatric critical care is a discipline driven by a steady stream of data which is acquired, analyzed, and synthesized to allow a rational and effective approach to care of critically ill and injured children. Algorithms and guidelines have evolved through efforts to improve outcomes by standardizing the approach to certain major pathophysiologic states. Accuracy and validity of the data measurements are essential elements of any critical care plan, and algorithms and pathways do not allow one to assume that data are correct. The practitioner must be aware of potential sources of error in measurement and interpretation, and be able to interpret data in context, considering the

common pItfalls and artIfacts In hemodynamIc monItorInG

Stephen R. Keller, MD, MHSA

entire picture of the patient rather than viewing the data as a collection of independent variables. In addition, complications associated with invasive monitoring must be clearly understood in order to rationally progress to goal-directed therapy based on measurements acquired in this way.

bLOOD PRessURe MONitORiNG

Blood pressure measurement is integral to support of the critically ill patient. Forward flow to vital organs, necessary for delivery of oxygen and substrate, and removal of waste, depends on the presence of a pressure gradient, or perfusion pressure. In the absence of such a gradient, no flow occurs. Establishment of an adequate pressure gradient is therefore paramount in support of the ICU patient.

invasive blood Pressure MonitoringArterial cannulation and transduction of pressure waveforms is considered the gold standard for monitoring of arterial pressure in the intensive care unit. Numerous technical issues can affect the accuracy of the measurement. These inaccuracies may become clinically significant, especially in the context of goal-directed therapy, in which control loop algorithms are used to titrate vasoactive therapy or intravascular volume manipulation. Also, it is not uncommon for discrepancies to occur between invasive and noninvasive measurements of blood pressure, resulting in confusion at the bedside over which number to use in directing therapy. A good understanding of the reasons for such discrepancies and for the potential sources of error in invasive measurements of blood pressure will allow rational resolution of these issues and application of appropriate interventions. Finally, the importance and limitations of blood pressure measurement as a representation of overall circulatory status in the critically ill child must be appreciated.

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Current Concepts in Pediatric Critical Care Refresher Course

technical sources Of errorPhysical properties of the system being measured have significant influence on the potential errors. The vascular system is complex, with periodic variations in pressure following each heart beat over a wide range of frequency. The high heart rate of infants was an issue in terms of responsiveness and fidelity of the transduced waveforms early in development of monitoring devices, but this has been addressed and generally is not a concern in modern PICU settings. A more difficult problem in accurate monitoring relates to the transmission of the pressure waveform down a progressively smaller, branching vascular tree with variable elastance and resistance depending on humoral and neural regulation of vascular tone. In clinical situations associated with increased resistance (e.g., hypovolemia, early compensated shock), reflection of kinetic energy back from the vascular tree to the end-hole vascular cannula can result in a higher measured systolic pressure which does not contribute to forward flow via a pressure gradient. An understanding of the physical concepts which follow can allow one to assess the accuracy of the data by analyzing the pulse waveform displayed on the monitor, prior to including it in goal-directed therapy.

Damping of the pulse waveform is associated with falsely low systolic pressures and falsely high diastolic pressures. The most common cause of this flattening of the waveform is vasospasm of the vessel in which the cannula lies. Technical problems, such as an air bubble in the fluid-filled tubing leading from the vascular cannula to the electronic transducer, or a loose connection in the tubing, may also cause this problem. The problem can be addressed by checking the tubing carefully for bubbles or loose connections. Once these have been eliminated, adding papaverine to the arterial line infusate is often helpful in reducing vasospasm at the site of the line insertion, which may result in a better waveform and more reliable pressure measurement. Finally, use of the mean arterial blood pressure (MABP) as a guide to therapy may be most appropriate. It is a function of the area under the arterial pulse waveform curve and is less affected by damping of the signal.

Resonance refers to the interaction between the natural frequency of a physical monitoring system and the frequency of the physiologic parameter being measured, such that erroneous waveforms and pressures are displayed. This waveform interaction is very similar to the interference displayed in the illuminated wave pool often performed in high school physics. The natural frequency of a tubing/transducer system is not dissimilar to that of a xylophone, so that the monitoring system itself may, with its intrinsic physical properties, influence the data generated. The modern ICU monitoring system is engineered to minimize these sources of error primarily by using stiff, noncompliant, narrow gauge, and short tubing. However, it is fairly common to see “fling” elevation of the systolic blood pressure, visible as a needle point projection at the peak of the pulse waveform, because the systems are set up to reduce damping of the signal. Once again, the mean arterial blood pressure is less affected by this phenomenon, so use of MABP in algorithms for goal-directed therapy may be more appropriate.

Finally, catheter whip due to movement within the vessel in a hyperdynamic circulatory state may impart kinetic energy to the end hole of the cannula, resulting in a higher pressure measurement. While this is not evident in small peripheral arteries, it may be a factor in catheters placed in larger central arteries or the aorta or pulmonary artery.

Noninvasive blood Pressure MonitoringMeasurement of blood pressure by noninvasive methods is commonly performed in the PICU setting. Because of the need for frequent repetitive measurement of blood pressure in critically ill children, the standard method using a sphygmomanometer and a stethoscope with auscultation of Korotkoff sounds has been largely supplanted by oscillometric automated devices integrated into the bedside monitor. Because either method depends on flow being present in the extremity being subjected to assessment, reliable data may be difficult to obtain in low-flow states. Less accurate measurement in alternate sites such as the leg, and by inferior methods such as the flush

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technique or Doppler detection of flow with manual decompression of the blood pressure cuff, are sometimes used until more accurate intravascular monitoring can be established.

It is important for the clinician to understand the differences between pressures measured by invasive versus noninvasive techniques. In each of these noninvasive methods, pressure is externally applied until flow ceases, and the blood pressure is then extrapolated from gradual release of that pressure until distension of compressed vessel walls occurs and flow is re-established and detected by various indicators. Conversely, with an invasive arterial line one is measuring a pressure head in a fluid medium with a static pressure and a kinetic energy component. The effect of the kinetic energy component is to make the measured intra-arterial systolic pressure 8-16 torr higher than the noninvasive measurement in the normal hemodynamic state, and up to 25-30 torr higher in patients with dramatically reduced vasomotor tone and hyperdynamic cardiac contractions such as are seen in sepsis (1).

Pitfalls in noninvasive blood pressure monitoring relate to 3 problems: 1) Data acquisition is intermittent rather than

continuous, making it more difficult to assess response to therapy with titration.

2) Severe vasoconstriction may make noninvasive blood pressure measurements unobtainable.

3) Cuff size must be appropriate to acquire accurate measurements. Since children vary widely in size, cuff selection is important. A cuff that is too small will result in blood pressures that are falsely high. Conversely, too large a cuff will underestimate blood pressure.The American Academy of Pediatrics (2) has recently revised recommendations for sizing of the cuff, such that the cuff length should approximate 40% of the circumference of the upper arm. A PICU study (3) comparing direct and indirect blood pressure measurements demonstrated that utilization of this recommendation

results in good correlation of systolic blood pressure (SBP) but consistent overestimation of diastolic blood pressure (DBP). These investigators also studied the comparison of direct intra-arterial measurement with the commonly used but obsolete upper arm length method (cuff width is two-thirds of upper arm length), and found consistent underestimation of both systolic and diastolic blood pressure, by means of 14.7 and 5.6 mm Hg, respectively.

Pressure Does Not equal FlowWhile establishment of adequate systemic blood pressure is central to the therapeutic plan, it does not guarantee that the primary goal is met, i.e., establishment of adequate oxygen delivery to the tissues. Flow, or cardiac output, is sometimes poorly reflected by blood pressure measurements because high systemic vascular resistance may maintain blood pressure in the normal range even in a low cardiac output state. Therefore, the clinician must not be reassured by the presence of a normal blood pressure. Measurement of flow is more complex, invasive, and subject to error, but is sometimes helpful in the clinical setting, and will be discussed in detail below.

DeteRMiNANts OF cARDiAc OUtPUt

Cardiac output is the product of stroke volume and heart rate. Determinants of stroke volume include preload, contractility, and afterload. Assuring adequate ventricular preload is the primary therapeutic intervention in pediatric shock, so accurate and reliable assessment of preload is highly desirable. Unfortunately, measurement of fiber length in the sarcomere at end-diastole, the most direct physiologic measure of preload, is not clinically feasible. Extrapolation from measurements that are clinically available is necessary. With each step away from direct measurement there is more potential error in measurement and interpretation. Contractility is also an extrapolated assessment in clinical practice, either derived from hemodynamic calculations or echocardiographic visual evidence involving

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measurements themselves subject to error. Afterload status may be clinically recognized by physical examination, qualitatively assessed if anatomic abnormalities or abnormal flow patterns are present by echocardiography or can be quantitatively calculated if pulmonary artery catheterization is performed. All methods are subject to errors in interpretation. Despite the difficulties in measurement and interpretation, such data can be successfully incorporated into goal-directed therapeutic algorithms with a holistic clinical approach leavened by knowledge of the pitfalls.

Preload AssessmentThe most commonly used measure of preload in pediatric critical care is the central venous pressure (CVP). As a right-sided pressure measurement being utilized to assess a remote left-sided volume parameter, left ventricular end diastolic volume (LVEDV), numerous factors may result in a misleading value. In pediatric patients, isolated left ventricular dysfunction not reflected in a high CVP measurement is unusual but must be kept in mind. Common conditions which might result in this picture include myocardial infarction related to anomalous left coronary artery arising from the pulmonary (ALCAPA) or Kawasaki disease with coronary aneurysms. Acute myocarditis or cardiomyopathy related to various metabolic disorders may also present with significant left ventricular (LV) dysfunction not necessarily reflected by a high CVP if right ventricular (RV) compliance is normal.

Another major factor affecting pressure measurements is ventricular compliance. A stiff ventricle, either on the right or the left side, may result in a high pressure even if the left ventricle is underfilled. Similarly, pericardial effusion with tamponade, constrictive pericarditis, or high pericardial pressure secondary to high ventilatory pressures may produce high filling pressures with low end-diastolic volume (4). Obstructions to left ventricular emptying such as aortic valvular stenosis produce a high end-diastolic pressure. Furthermore, any anatomic or pathophysiologic

cause of increased resistance to left ventricular filling situated between the tip of the catheter and the left ventricular chamber may result in misleading high pressure readings suggesting adequate preload is present. On the left side, these include mitral valve disease and pulmonary venous obstruction. On the right side, pulmonary hypertension, pulmonary embolus, pulmonic valve disease, right ventricular dysfunction, intracardiac left–to-right shunt, tricuspid valve disease, or thrombus in the vein in which the catheter is placed all may obfuscate the true volume status of the left ventricle by producing high pressure measurements.

Despite all these potential pitfalls the CVP remains a useful measurement in pediatric critical care because in many cases the value is low, prompting the correct initial intervention of intravascular volume expansion. Observation of the response to volume expansion with continuous monitoring of the CVP can help identify adequate volume loading and prompt addition of inotropic support. An initial high value, on the other hand, should prompt further thought and evaluation. Echocardiography can be very helpful in this situation, to look for anatomic or flow abnormalities explaining the high pressure, to assess intracardiac chamber size for adequate filling, and to obtain an assessment of contractility.

In addition, knowledge of normal and abnormal waveform patterns can be helpful and often diagnostic of problems leading to high venous pressure with low cardiac output. Examples include: 1) cannon waves seen in a-v dissociation resulting in atrial contraction against a closed cardiac valve; 2) late cannon waves of tricuspid insufficiency; and 3) narrow pulse pressure waveform seen in pericardial tamponade.

Pulmonary artery occlusion pressure (PAOP) measurement via placement of a pulmonary artery catheter (PAC) may allow more accurate assessment of left ventricular preload because the appropriately measured value correlates well with left atrial pressure and eliminates

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some of the confounding variables involved in CVP interpretation. Although pulmonary artery catheterization is rarely performed in pediatric critical care in 2005, it is important for pediatric intensivists to become familiar with the risks and pitfalls in interpretation associated with this monitoring modality. For the occasional patient subjected to this procedure, there is more risk of misinterpretation and incorrect interventions due to lack of experience.

Risks of PAC placement include ventricular arrhythmias triggered by the catheter as it passes through the right ventricle, perforation of the heart resulting in tamponade, pulmonary infarction due to inadvertent wedging of the catheter in a branch of the pulmonary artery, formation of thrombus on the catheter, and infection including endocarditis.

The assumption may be made that pulmonary artery occlusion pressure accurately reflects intravascular volume status and left ventricular preload. However, PAOP may be high if there is mitral valve disease or LV dysfunction with decreased compliance, prompting the potentially incorrect conclusion that fluid resuscitation has been adequate or excessive.

Airway pressure is another very important factor in interpretation of the PAOP in patients receiving positive pressure ventilatory support. Proper placement of the catheter in West Zone III (posterior segments of lower lobes for the supine patient, with higher levels of blood flow) to achieve a continuous fluid column between the catheter tip and the LV, is important in obtaining reliable PAOP measurements as an indirect reflection of left ventricular preload. Placement in upper lobes or anterior segments with relatively more inflation of alveoli than pulmonary blood flow, West Zone I, will exaggerate the effect of positive pressure ventilation on the measurement, creating a misleading high value. This effect results from high levels of positive pressure ventilatory support, which may increase pulmonary vascular resistance due to compression of the pulmonary vascular bed or reflex vasoconstriction. In addition, if during

the respiratory cycle alveolar airway pressure exceeds pulmonary venous pressure, thereby interrupting pulmonary blood flow through vascular compression, high levels of positive ventilatory pressure may convert the monitored lung site from optimal West Zone III to Zone II (lower flow to ventilation ratio) despite proper initial placement of the catheter tip in a dependent lower lobe. This pitfall may be avoided by careful measurement of PAOP at end-expiration as judged by observation of respiratory variation in the pressure tracing printout. Another non-intuitive source of error is that, paradoxically, aggressive diuresis resulting in hypovolemia may cause the conversion of Zone III lung physiology to that of Zone II, causing misleadingly high PAOP in volume-depleted patients on high levels of PEEP. Finally, surgically placed transthoracic left atrial catheters are used to measure left atrial pressure (LAP) in postoperative pediatric cardiac surgery patients to allow a more direct assessment of LV function and preload in the setting of pulmonary hypertension, selective LV dysfunction, or other factors which might create falsely high CVP readings in the setting of an underfilled left ventricle. With all the clinical bedside measures of intravascular volume status, it is important to recognize the optimal value that supports adequate cardiac output for the individual patient, considering all confounding variables, rather than aiming for a generic standard value. For example, for a postoperative patient following complete repair of Tetralogy of Fallot, the CVP may need to be in the mid-teens (well above the “normal” range) in order to support cardiac output, because of the effect of longstanding right ventricular hypertrophy resulting in decreased RV compliance. Another common scenario for inadequate cardiac filling despite high central venous pressure measurement involves a patient with high mean airway pressure (MAP), either with conventional mechanical ventilation or with high-frequency oscillatory ventilation. This may occur because systemic venous return is inhibited by the high intrathoracic pressure. Also, increased RV afterload produced by increased pulmonary vascular resistance secondary

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to high levels of ventilatory support may result in RV dilatation causing interventricular septal shift to the left compromising LVEDV and stroke volume.

contractility AssessmentContractility is defined as the velocity of myocardial fiber shortening, a measurement impossible to achieve in the clinical setting. Therefore, evaluation of contractility is intermittent, indirect, and subject to interpretive error. The most common assessment in the PICU is by 2-D echocardiography. Estimation of shortening fraction or ejection fraction is inherently inaccurate because the measurement is made 2-dimensionally, while accurate estimation of stroke volume would require a 3-dimensional measurement. In addition, any of the measurements approximating stroke volume as a marker of contractility are subject to the influence of afterload and valvular regurgitation. High afterload secondary to valvular stenosis or increased systemic vascular resistance will decrease stroke volume even with normal contractility, while pharmacologic vasodilation can increase stroke volume even with poor contractility. Valvular regurgitation may effectively reduce afterload allowing a large stroke volume, partially in the wrong direction with a net result of inadequate systemic flow.

Estimations of contractility via nuclear medicine scans or calculations based on data derived from thermodilution pulmonary artery catheters are subject to the same confounding factors and are less available in the PICU setting, so they are rarely used.

Afterload AssessmentVentricular afterload is difficult to assess in a precise or continuous fashion, so it tends to be followed clinically via physical examination of pulses, surface temperature and color, and capillary refill. Systemic and pulmonary vascular resistance can be calculated from pulmonary artery catheter thermodilution and hemodynamic data, but these are rarely available. Measurement of pulmonary artery pressures (PAP) can be carried out continuously with a transthoracic catheter placed in surgery for

congenital cardiac repair, allowing recognition of pulmonary hypertensive crises and evaluation of response to therapy with inhaled nitric oxide or other interventions. One pitfall in interpretation of a high PAP is that high flow due to left-to-right shunt may produce a high pressure even in the presence of normal pulmonary vascular resistance. Echocardiographic data estimating resistance via flow patterns is available only intermittently and is subject to error, so it is not a practical component of goal-directed therapy. However, anatomic defects causing increased afterload, such as valvular aortic stenosis, can be appreciated by echocardiography, which allows judicious application of therapeutic interventions.

cardiac Output AssessmentAssessment of cardiac output in the PICU setting is challenging and subject to a variety of potential errors. Invasive measurement by green-dye dilution, a mainstay of assessment in the early days of open heart surgery, has been supplanted by thermodilution utilizing a pulmonary artery catheter. Both techniques actually measure venous return rather than systemic output. Thermodilution is not subject to the recirculation issue intrinsic to green dye dilution, since the room-temperature saline is fully normalized to body temperature in the first pass through the lungs. The technique can be fairly accurate and reproducible in experienced hands, but is subject to operator variation, computational errors, and is based on the assumption that there is no intracardiac shunt through septal defects. Other confounding conditions which may invalidate the measurement include tricuspid regurgitation, atrial arrhythmias, and variation in timing of the respiratory cycle with indicator injection. Operator variation can be addressed by performing 3 separate injections and measurements to demonstrate concordance of the results. The variation can be so significant that the clinician often averages the best 2 out of 3 results. Frequent injection of large volumes of saline is problematic in small children due to potential fluid overload. Finally, the measurement is only intermittent at best, so that moment-to-moment changes in patient status or responses to titration of therapy may not

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be appreciated. Femoral artery thermodilution has been compared to clinical assessment in infants and children following open-heart surgery in a small study, which showed superiority of the method to clinical assessment by nurses and physicians in recognition of hypovolemia and increased systemic vascular resistance (5). This method eliminates many of the risks associated with pulmonary artery catheterization, but has not been studied sufficiently to document improvement in outcomes justifying the cost and risk of limb ischemia in placement of the catheter, so has not been widely adopted.

Direct measurement of oxygen consumption, arterial oxygen content, and mixed venous oxygen content can be utilized to calculate cardiac output via the Fick principle (Cardiac output=O

2

consumption/CaO2-CmvO

2); however, accurate

bedside measurement of O2 consumption is

difficult, and small errors in measurement can produce large errors in computed cardiac output, rendering this method impractical.

Echocardiography provides a noninvasive, indirect approach to assessment of cardiac output, but is subject to significant errors as well. For example, flow estimation depends on the cross-sectional area of the vessel being evaluated; a high flow across a narrow vessel may not represent adequate output. Also, measurements of ejection fraction and shortening fraction may suggest a higher systemic output than exists due to mitral valve regurgitation or aortic insufficiency. Continuous transesophageal echocardiography has been adopted for monitoring adults in some venues (6), but has not gained acceptance in pediatric centers. New technology exists that offers continuous assessment of cardiac output via measurements of beat-to-beat variations in thoracic bioimpedance (7) or by analysis of the arterial pulse waveform (8), but these have not yet gained wide acceptance and application in the pediatric intensive care setting.

Continuous or intermittent sampling of mixed venous oxygen saturation provides an indirect measure of the adequacy of tissue oxygen delivery, which with normal oxygen consumption should

result in a venous saturation of around 75%. Low venous saturations coupled with high arterial saturations signify inadequate delivery of O

2 to

meet the metabolic demand. This may correlate to low cardiac output, inadequate arterial oxygen content, or excessive oxygen demand due to a hypermetabolic state. Therefore, pitfalls in interpretation of this data include the possibility of anemia, abnormally high oxygen consumption, or abnormal hemoglobin, which can present the same pattern as low cardiac output. High venous O

2 saturation may be seen if intracardiac shunting

is present, rendering venous oximetry useless as an indirect monitor of cardiac output. Extracardiac a-v shunting (seen in sepsis) or metabolic blockade of electron transport, such as with cyanide, may cause poor oxygen uptake and utilization in the tissue beds not related to the adequacy of oxygen delivery.

Measurement of oxygen delivery and consumption has been studied as a guide to therapeutic interventions in adult patients (9). In pediatrics, the risk-benefit ratio of pulmonary artery catheterization has not been established with respect to optimization of oxygen delivery as a therapeutic goal, nor have specific optimal goals been established. Pitfalls in interpretation include a-v shunting, uncoupling of oxygen transport and energy generation, and use of derived variables with inherent potential inaccuracy in measurements and assumptions.

capnographyMonitoring of end-tidal CO

2 (ETCO

2) has potential

utility as an early warning system for decreasing cardiac output, since alveolar CO

2 depends on

delivery by adequate pulmonary blood flow. As cardiac output decreases to a critical level, exhaled CO

2 also falls. Adequacy of resuscitative efforts

will be reflected in the rise of ETCO2 in exhaled

gases. Pitfalls in interpretation are revealed when arterial blood gases are performed showing a gap between paCO2 and ETCO

2, and include:

1) severe airway or parenchymal lung disease causing significant ventilation-perfusion mismatch, resulting in dead-space ventilation and a false low ETCO

2 value; 2) false low value because of failure

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to obtain a true alveolar sample due to expiratory obstruction. Airway obstruction can be recognized by evaluation of the capnograph waveform, which does not achieve a plateau, but instead continuously rises until end expiration.

Metabolic Parameters As indications Of Adequate tissue Perfusion And O

� Delivery

Many investigators have studied indicators of end-organ function or tissue metabolism as hemodynamic monitoring parameters. While these indicators have some theoretical appeal, each is limited by confounding variables, technical unavailability, or lack of pediatric studies or experience. Most prominent and widely used of these is the serum lactate. It has been shown to correlate to mortality risk in certain groups such as postoperative cardiac surgery patients (10), and in children with shock (11). Goal-directed therapy using serial lactate determinations in postoperative pediatric cardiac surgery patients has been reported to be improve outcome, especially in younger, more high-risk patients (12). The use of serum lactate as an indicator for goal-directed therapy has not been widely adopted to date, partly because modification of therapy based on the lactate level requires rapid turnaround probably best achieved, as in this study, by point-of-care testing at the bedside. Base deficit has been clinically used for many years as an indicator of ongoing tissue acidosis, but as shown by Murray et al (13) there is a poor correlation of this calculated value with presence of unmeasured organic acids and tissue lactate. Similar lack of rapid expression of inadequate perfusion and tissue hypoxemia, as well as lack of specificity, underlie the lack of utility of serum creatinine and liver function parameters as monitors of hemodynamic status.

Gastric tonometry has been studied extensively in adults as an indicator of adequacy of splanchnic tissue oxygen delivery as a proxy for hemodynamic status (14). Unfortunately there are technical limitations and confounding results in the limited studies on children utilizing this technology (15), so it has not been widely adopted in the PICU setting.

ReFeReNces

1. Swedlow DB, Cohen DE. Invasive assessment of the failing circulation. In: Swedlow DB, Raphaely RC (eds). Cardiovascular Problems in Pediatric Critical Care; Clinics in Critical Care Medicine. New York, Edinburgh, London, Melbourne: Churchill Livingstone; 1986: 129-168.

2. National High Blood Pressure Education Program Working Group on Hypertension Control in Children and Adolescents. Update on the 1987 Task Force Report on High Blood Pressure in Children and Adolescents: A Working Group Report from the National High Blood Pressure Education Program. Pediatrics. 1996;98(4):649-658.

3. Clark JA, Lieh-Lai MW, Sarnaik A, Mattoo TK. Discrepancies between direct and indirect blood pressure measurements using various recommendations for arm cuff selection. Pediatrics. 2002;110(5):920-923.

4. Pinsky MR. Clinical significance of pulmonary artery occlusion pressure. Intensive Care Med. 2003;29:175-178.

5. Egan JR, Festa M, Cole AD, et al. Clinical assessment of cardiac performance in infants and children following cardiac surgery. Intensive Care Med. 2005;31:568-573.

6. Poelaert JI, Schupfe G. Hemodynamic monitoring utilizing transesophageal echocardiography: the relationships among pressure, flow, and function. Chest. 2005;127(1):379-390.

7. Tibby SM, Murdoch IA. Monitoring cardiac function in intensive care. Arch Dis Child. 2003;88:46-52.

8. Piehl, MD, Manning J, McCurdy SL, et al. Comparison of pulse contour analysis with pulmonary artery thermodilution in a pediatric model of hemorrhagic shock. [Abstract]. 2004 Pediatric Critical Care Colloquium, New York, NY. Available at: http://pedsccm.wustl.edu/ORG-MEET/PCCC2004/PCCC_2004_abstracts.htm.

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9. Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS. Prospective trial of supernormal values of survivors as therapeutic goals in high-risk surgical patients. Chest. 1988;94:1176-1186.

10. Siegel LB, Dalton HJ, Hertzog JH, et al. Initial postoperative serum lactate levels predict survival in children after open heart surgery. Intensive Care Med. 1996;22(12):1418-1423.

11. Hatherhill M, Waggie Z, Purves L, Reynolds L, Argent A. Mortality and the nature of metabolic acidosis in children with shock. Intensive Care Med. 2003;29:286-291.

12. Rossi AF, Khan DM, Hannan R, et al. Goal-directed medical therapy and point-of-care testing improves outcomes after congenital heart surgery. Intensive Care Med. 2005;31:508-509.

13. Murray DM, Olhsson V, Fraser JI. Defining acidosis in postoperative cardiac patients using Stewart’s method of strong ion difference. Pediatr Crit Care Med. 2004;5:240-245.

14. Heard SO. Gastric tonometry: the hemodynamic monitor of choice-pro. Chest. 2003;123(5Suppl):469S-474S.

15. Thorburn K, Durward A, Tibby SM, Murdoch IA. Effects of feeding on gastric tonometric measurement in critically ill children. Crit Care Med. 2004;32(1):246-249.

ADDitiONAL ReADiNG

Adatia I, Cox PN. Invasive and noninvasive monitoring. In: Chang AC, Hanley FL, Wernovsky G, Wessel DL (eds). Pediatric Cardiac Intensive Care. Baltimore, MD: Williams and Wilkins; 1998: 137-147.

Bohn D. Cardiopulmonary Interactions. In: Chang AC, Hanley FL, Wernovsky G, Wessel DL (eds). Pediatric Cardiac Intensive Care. Baltimore, MD: Williams and Wilkins; 1998: 107-125.

Hung DT, Lilly CM. Making the most of hemodynamic monitoring in the ICU: observing and optimizing appropriate parameters. J Crit Illness. 2003;18(5):196.

Perloff WH. Invasive measurements in the PICU. In: Fuhrman B, Zimmerman J (eds). Pediatric Critical Care. 2nd edition. Elsevier: 1998:67-98.

Schieber RA. Noninvasive recognition and assessment of the failing circulation. In: Swedlow DB, Raphaely RC (eds). Cardiovascular Problems in Pediatric Critical Care; Clinics in Critical Care Medicine. New York, Edinburgh, London, Melbourne: Churchill Livingstone; 1986: 87-127.

Swedlow DB. Noninvasive respiratory gas monitoring. In: Fuhrman B, Zimmerman J (eds). Pediatric Critical Care. 2nd edition. Elsevier: 1998:99-110.

Common Pitfalls and Artifacts in Hemodynamic Monitoring

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