Hemodynamic Monitoring in the Intensive Care Unit

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2012 27: 340Nutr Clin PractJoseph C. Muller, Jason W. Kennard, Jeffrey S. Browne, Alison M. Fecher and Thomas Z. Hayward

Hemodynamic Monitoring in the Intensive Care Unit

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Nutrition in Clinical PracticeVolume 27 Number 3June 2012 340-351© 2012 American Society for Parenteral and Enteral NutritionDOI: 10.1177/0884533612443562http://ncp.sagepub.comhosted athttp://online.sagepub.com

Invited Review

Hemodynamic monitoring is the observation of physiologic parameters of the cardiovascular system. The purpose of the cardiovascular system is to transport substrates and oxygen to the cells throughout the body and to ensure adequate cellular function. Inadequate tissue perfusion and oxygenation is a common definition of shock. Eventually, without resuscitation, the shock state leads to multiple-organ dysfunction syndrome and death. The purpose of hemodynamic monitoring is to observe that adequate mean arterial pressure, tissue perfusion, and oxygen delivery remain adequate. Traditionally, hemody-namic monitoring information has been derived from invasive catheters.

The purpose of this article is to review how, in the current intensive care unit (ICU), hemodynamic monitoring is com-monly performed. A basic understanding of how monitoring is accomplished, how the data are interpreted, and how that inter-pretation leads to changes in clinical care should be of interest to the nutrition support professional because one of the basic tenets of care of the critically ill or injured is the basic priority scheme. The priorities are always airway, breathing, and circu-lation. Usually, by the time the nutrition support professional gets involved, airway and breathing have been addressed. The patient is commonly intubated and on the ventilator in the ICU. However, circulation is often a work in progress. The difficulty for the nutrition support professional is that his or her recom-mendations for nutrition will depend on how the patient is doing physiologically. Although there is a wide spectrum as to how aggressively enteral nutrition (EN) vs parenteral nutrition (PN) will be pursued, there are limits to the patient’s ability in shock states to respond to either. To understand how well or

poorly resuscitated the patient is depends on the data from hemodynamic monitors and the clinician’s judgment. The key question that the nutrition support professional needs to ask is, “Is this patient in a state of shock?” As with most diagnoses, identifying the problem is the first step. The next step in resusci-tation is to develop a treatment plan to improve the patient’s con-dition. The last step is to monitor and verify that the shock state has resolved and the patient’s condition continues to improve.

The problem with this model is that no hemodynamic moni-toring system currently available can directly measure tissue hypoxia at the cellular level. Rather, monitored physiologic variables are an estimate of the physiology. These estimates are then used clinically to provide and direct therapeutic deci-sions, thereby benefiting the patient. However, monitoring in and of itself does not improve patient outcomes. The monitor-ing of hemodynamic data combined with the clinician’s bed-side assessment of the patient can generate interventions that improve clinical outcomes.1 The corollary is also true as fail-ure in interpreting the data can lead to poor outcomes as well. Therefore, the clinician must be familiar with the strengths and weaknesses of each hemodynamic monitor under a variety of pathologic conditions so as to interpret the data correctly and reliably. Failure in interpretation of the hemodynamic data can

443562 NCPXXX10.1177/0884533612443562Hemodynamic Monitoring in the Intensive Care Unit / Muller et alNutrition in Clinical Practice2012

From Indiana University School of Medicine, Indianapolis, Indiana.

Financial disclosure: none declared.

Corresponding Author: Thomas Z. Hayward, Indiana University School of Medicine, 1001 10th street, Meyers 1014, Indianapolis, IN 46202; e-mail: [email protected].

Hemodynamic Monitoring in the Intensive Care Unit

Joseph C. Muller, MD; Jason W. Kennard, MD; Jeffrey S. Browne, MD; Alison M. Fecher, MD; and Thomas Z. Hayward, MD, MBA

AbstractPatients in the intensive care unit are often critically ill with inadequate tissue perfusion and oxygenation. This inadequate delivery of substrates at the cellular level is a common definition of shock. Hemodynamic monitoring is the observation of cardiovascular physiology. The purpose of hemodynamic monitoring is to identify abnormal physiology and intervene before complications, including organ failure and death, occur. The most common types of invasive hemodynamic monitors are central venous catheters, pulmonary artery catheters, and arterial pulse-wave analysis. Ultrasonography is a noninvasive alternative being used in intensive care units for hemodynamic measurements and assessments. (Nutr Clin Pract. 2012;27:340-351)

Keywordshemodynamics; intensive care; intensive care units; critical care; catheterization, Swan-Ganz; pulmonary wedge pressure; ultrasonography

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Hemodynamic Monitoring in the Intensive Care Unit / Muller et al 341

lead to poor outcomes, just as correct interventions can lead to improved outcomes.

The principal hemodynamic monitors used in clinical prac-tice today are central venous catheters, pulmonary artery cath-eters, and arterial pulse-wave analysis. A central venous catheter is an invasive catheter placed in a central vein of the neck or shoulder with its tip lying at the superior vena cava/right atrium junction. A pulmonary artery catheter is a longer central venous catheter with multiple ports and extends from the central vein through the superior vena cava, right atrium, right ventricle, and into the pulmonary artery. Arterial pulse-wave analysis refers to an arterial catheter hooked up to a com-puter running an algorithm to assess beat-to-beat pulse variability in arterial resistance and compliance. Ultrasound at the bedside in the ICU evaluates the hemodynamics at one time point, thereby better directing the use of more invasive monitors. This noninvasive evaluation is limited by technique and patient anatomy.

Central Venous Pressure

A common invasive line used in the ICU is a central venous catheter. There are many uses for such a line: blood draws, medication administration, PN, and monitoring of central venous pressure. The trending of pressure readings can be used to determine different physiological variables that are occurring in the circulatory system just proximal to the heart.

Central venous pressure (CVP) is defined as the back pres-sure to systemic venous return. It is measured at the level of the right atrium with the help of a central line placed in the vena cava. As the heart is continuously beating, a CVP waveform will be present, which can lead to different values of CVP depending on which point of the waveform is analyzed (see Figure 1). This leads to 3 different “waves” (a, c, and v) and 2 different “descents” (x and y). The “a” wave represents atrial contraction that occurs after the p wave of the standard cardiac electrocardiogram (ECG) tracing. The “c” wave represents buckling of the tricuspid valve as it closes due to ventricular systole. The slow-rising “v” wave represents filling of the atrium during diastole. The correct CVP equals the right- ventricular end-diastolic pressure (RVEDP). The RVEDP occurs when the tricuspid valve is open and the right ventricle is filled just prior to contraction. In the waveform (see Figure 1), this occurs between the “a” wave and the “c” wave, at the valley in between the 2 letters. In addition, these values should be measured at the end of an expiratory cycle, as intrathoracic pressures from ventilation affect the CVP (see Figure 1).

In the late 19th century, Otto Frank investigated the rela-tionship between the stretched length of a muscle and its con-tractile strength. He was able to determine that the contractile strength of heart muscle was increased when the muscle was stretched. In the early 20th century, Ernest Starling and his group published their studies that increasing the venous return to the heart of dogs subsequently increased the stroke volume.

Their combined work is now called the Frank-Starling mecha-nism, which states that under normal physiologic conditions, the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (see Figure 2).2

Because the filling pressure of the left heart is dependent on the output of the right heart through the pulmonary circulation, the filling pressure of the left ventricle is dependent on CVP as a factor in determining its preload. Therefore, CVP has been (and often still is) used as a marker to determine the preload or filling pressure of the heart.

CVP can be measured by a bedside evaluation and looking at the level of distention (or lack thereof) of a patient’s jugular veins. Commonly, CVP is obtained with transducers through the distal port of a central line lying at the junction of the supe-rior vena cava (SVC) and the right atrium. The midaxillary line of the chest at the fifth intercostal space is commonly used as an anatomical landmark to determine the level of the right atrium, where the transducer is zeroed. Ideally, the patient should be supine for the measurement. If clinically necessary, the head of the bed can be elevated as long as the transducer is positioned in the same place each time and the angle of the bed remains the same.

For better or worse, CVP is used as a marker of preload and adequate resuscitation. Normal CVP has a large range but is typically valued at 0–8 mm Hg. In certain clinical conditions, CVP can help guide fluid management and interventions to attempt to maximize preload. In the Frank-Starling mechanism outlined above, it is important to realize that there is a plateau in the graph. As preload continues to increase above a certain point, there is no improvement in stroke volume. This

Figure 1. Central venous pressure (CVP) waveform as it relates to an electrocardiogram cycle. The CVP should be measured at end diastole, marked as the valley between the “a” and “c” waves.




342 Nutrition in Clinical Practice 27(3)

transition point varies with disease processes, patients, and even the same individual at different time points.

Several studies in the literature give a target value of CVP depending on certain clinical conditions. For instance, in the Surviving Sepsis Campaign guidelines,3 rapid resuscitation to a target CVP of 8–12 mm Hg is recommended for patients in severe sepsis and septic shock. This stems from the landmark article by Rivers et al,1 which showed a significant reduction in mortality in these patients if they were resuscitated to this level. During liver surgery, it is common practice to lower the CVP below 5 mm Hg to minimize intraoperative blood loss.4 Studies have also shown that a CVP of 4–9 mm Hg reduces air embolization during neurosurgical procedures in the semi-sitting position.5

A CVP measurement can be viewed in 2 basic ways: static measurements and dynamic monitoring. Looking at a single measurement at a point in time is a “static” measurement. Little clinical information can be gained from a static mea-surement of CVP because there is no context. A better way is to incorporate CVP monitoring as a “dynamic” monitor—for example, trending the CVP measurements over time and evaluating how the CVP and other hemodynamic values change in response to a stimulus, most often a fluid chal-lenge. A fluid challenge is not the same as volume resuscita-tion. It is merely a marker for those who are preload responsive and may benefit from continued fluid resuscita-tion to help improve hemodynamic indices.6 Finally, only 50% of all hemodynamically unstable patients will be pre-load responsive.7 Although a fluid challenge is a common first step in resuscitation, other interventions (pressors,

inotropes, steroids, blood, etc) are often needed to effectively resuscitate a critically ill patient.

For all the information that can be gathered by CVP moni-toring, there are flaws inherent within the system. First, CVP requires an invasive line to be placed in the central venous sys-tem, which carries with it complications. Up to 15% of patients experience 1 or more complications from central line inser-tion.8,9 Some common mechanical complications that arise after the attempted placement of central venous catheters include arterial puncture, pneumothorax, hemothorax, and car-diac arrhythmias. More serious complications that can arise after placement include venous or cardiac perforation, cardiac tamponade, venous air embolism, and even death. More com-monly, infectious complications arise with indwelling vascular catheters, which can also be life-threatening.

Second, a CVP measurement is typically a small number, and very small inaccuracies in measurement can influence fur-ther treatment strategies. Figg and Nemergut10 demonstrated that when different practitioners who were experienced in dealing with central lines were left to zero a transducer to the level of the right atrium and then measure a CVP, their mea-surements differed by as much as 17 cm H

2O with a standard

deviation of 4 cm H2O. This, according to the ICU protocols

and guidelines, could mean the difference between aggressive fluid resuscitation and giving a diuretic. Even when the trans-ducer is set and an electronic monitoring device prints out a CVP waveform recording for a board-certified ICU doctor to analyze, interphysician disagreements of more than 2 mm Hg occur 24% of the time, and 7% of the time the difference is over 5 mm Hg.11 When these results were theoretically tied into goal-directed therapy, therapy would have been altered in over 20% of the patients depending on which CVP measure-ment was used.

Finally, it is important to realize that using CVP as a marker of left ventricular preload depends on several assumptions. It assumes that pulmonary resistance and right heart function are normal and unimpaired and that intrathoracic pressures do not vary significantly. The body does many different things to maintain homeostasis when critically ill, individually affecting the CVP required for optimal cardiac function.12 Variability of cardiac pump function and vascular resistance directly affect the optimal CVP for maximal cardiac output. For instance, there can be changes in arterial blood pressure, vascular resis-tance, and venous capacity simply by inducing the carotid body reflex, which is a homeostatic feedback mechanism caused by the stretch of the baroceptors in the carotid body, without any significant changes in the CVP.13 Magder14 points out that it is impossible to take into consideration CVP alone without also assessing cardiac output and tissue perfusion.

CVP monitoring has long been available for management of critically ill and injured patients as a rough marker for car-diac preload. Despite its limitations, it is readily measureable from a central venous catheter as long as proper measurement

Figure 2. Graphical representation of the Frank-Starling mechanism. As preload (end-diastolic volume) increases, stroke volume increases. The entire curve can be moved due to changes in heart contractility. CVP, central venous pressure; ECG, electrocardiogram.





techniques are undertaken. It is best used as a dynamic, rather than a static, measurement. These values should be taken in context with other physiologic parameters for the patient to help guide clinical fluid management. It can be a helpful marker in discriminating the different types of shock.

The Pulmonary Artery Catheter

Swan and Ganz15 first described the pulmonary artery catheter (PAC) in 1970. Since that time, the medical literature has her-alded the PAC as both life-saving as well as life-threatening, and the popularity of the technology has followed suit and vacillated over the ensuing years.

After the PAC introduction, it soared in popularity through the 1980s. An observational study of PAC use in the setting of acute myocardial infarction (AMI) mirrored the growing trend across the nation. During the 4 years studied (1975, 1978, 1981, and 1984), incidence in the setting of AMI in which PACs were thought to be indicated grew: 7.2% initially, then 13.8%, then 14.8%, and eventually 19.9%, respectively.16 A 1984 prospective study of 142 consecutive autopsies revealed that 55 patients (39%) died with a PAC in place.17

As PAC popularity grew, the need for evidence of its effi-cacy through prospective, randomized trials was demanded.18 Connors et al19 answered this call in 1996. Their study found increased cost, length of stay, and, most important, mortality (odds ratio, 1.24) among 5735 case-matched and prospectively analyzed critically ill patients. As a result of the findings in the Connors et al study, the PAC became the focal point of a num-ber of randomized trials spanning different critically ill patient populations (medical, surgical, shock, adult respiratory dis-tress syndrome [ARDS]). Ultimately, the studies concluded that the PAC did not improve outcomes, while placing patients at risk for catheter-related complications.19-25

As evidence amassed against its benefit, PAC use decreased by 65% between 1993 and 2004 (5.66 to 1.99 per 1000 medical admissions in 1993 and 2004, respectively).26 The studies reevaluating the PAC, however, were themselves criticized due to design flaws, selection biases, and ethical considerations. Ethically, the question of whether a physician believing some-one could benefit from a PAC could randomize that person to a study arm disallowing that technology was raised. This was felt to have led to the exclusion of those patients in which the PAC would have been most beneficial in many studies.

The studies were also criticized for a near-universal lack of inclusion of the PAC in a treatment algorithm.27 This changed in 2006 with a study published courtesy of ARDSnet. The Fluid and Catheter Treatment Trial (FACTT) compared mor-tality, ventilator-free days, and ICU stay among patients diag-nosed with acute lung injury (ALI). A total of 1000 randomized patients received either central venous catheter (CVC)–directed resuscitation (measuring CVP) or PAC-directed resus-citation (measuring cardiac index [CI] and pulmonary artery occlusion pressure [PAOP]). The study found no significant

benefit to PAC in PAC-directed resuscitation (mortality: 27.4% [CVC] vs 26.3% [PAC], P = .69; ventilator-free days: 13.2 [CVC] vs 13.5 [PAC], P = .58; days not spent in the ICU: 12.0 [CVC] vs 12.5 [PAC], P = .40).28 The widespread use of the PAC decreased markedly after the FACTT publication.

Currently, consensus guidelines are largely based on expert opinion because randomized data supporting pulmonary artery catheter usage are lacking. The consensus statements available are from the 1997 Society of Critical Care Medicine (SCCM) Pulmonary Artery Catheter Consensus Conference as well as the 2003 American Society of Anesthesiologists (ASA) Practice Guidelines for Pulmonary Artery Catheterization.29,30 The clinical settings indicating PAC use are listed in Table 1.

Beyond the medical indications for PAC use and nursing familiarity with the PAC, its setup and methodology for obtaining hemodynamic data remain a critical aspect of its use. Nursing scores on basic PAC fund of knowledge assess-ment tools among critical care nurses remain consistently low around the world (42.5%–56.8% correct answers).31-33 This is a result of their infrequent use. Further, ASA guide-lines state that perioperative indications for PACs should be based on whether nursing in that facility is familiar with PAC monitoring.30

Similarly, physician competence necessary for PAC use has been disappointing. In 1997 Trottier and Taylor34 published the results of a survey of SCCM members, revealing that 33% of responders could not properly identify PAOP on a clearly marked tracing. A physician lacking detailed knowledge of PAC use, insertion techniques, troubleshooting, and waveform interpretation should not endeavor to insert this device.

Insertion of a PAC begins by inserting a 9-French intro-ducer sheath into a central vein. The PAC is then inserted through the introducer sheath into the central vein. A 1.5-mL balloon tip at the end of the PAC is used to direct the catheter from the central vein through the SVC, right atrium, right ven-tricle, and into an occlusive “wedge” position in the pulmo-nary artery (Figure 3). The PAOP can then be carefully measured (Table 2). PAOP tracings vary with respiration. It is for this reason that interpretation of the PAOP is a learned skill. End expiration is used as the point of measurement because at this point in the respiratory cycle, intrathoracic pressure approximates atmospheric pressure. This holds true for both mechanically ventilated and spontaneously breathing patients (Figure 4).

In the wedge position, PAOP is correlative with a number of hemodynamic measurements aligned in series: the pulmonary artery (PA) pressure distal to the occlusive “wedge” position, pulmonary capillary (PC) pressure, pulmonary vein (PV) pres-sure, left atrial (LA) pressure, and the left ventricular end- diastolic pressure (LVEDP). Taking the example of a river, downstream obstruction by the construction of a dam has the consequence of upstream flooding. In vivo, acute left heart failure produced by pathologies such as AMI can serve as a surrogate for the dam. Upstream flooding becomes realized as





flow backs up (hence, pressures rise) throughout the upstream circuit from the left ventricle to the elevated PAOP. A normal PAOP suggests that there is no obstruction or resistance to nor-mal flow and effectively rules out a cardiac cause of pulmo-nary edema. It is for this reason that a normal PAOP <18 is necessary to rule out a cardiogenic cause of lung disease prior to making the diagnosis of ARDS.35

LVEDP is correlative with left ventricular end-diastolic volume (LVEDV), assuming normal cardiac compliance. Therefore, if a patient has increased preload (eg, by giving a 0.9% normal saline bolus), it will be reflected as an increased LVEDP and LVEDV. As myocardial fibers stretch (LVEDV increases) at the microscopic level, contractility (stroke vol-ume) improves up to a point in a relationship known as the Frank-Starling curve (which was previously discussed). Increasing preload, then, is a surrogate marker for improved stroke volume, cardiac output (CO), and cardiac index (CI). An accurate assessment of preload is integral to the establishment of a critically ill patient’s volume status. The PAOP is therefore viewed as a tool to assist the critical care physician in this assessment.36,37

A patient’s progression along the Frank-Starling curve can be assessed by PAOP. Pulmonary artery catheters provide CO and CI data using the principle of thermal dilution. Branthwaite and Bradley38 first directly measured CO in human partici-pants using thermal dilution in 1968. The mathematical equa-tion applied to calculate CO by thermal dilution (the Stewart-Hamilton equation) is complex,39 but its concept is quite eloquent. Thermal dilution relies on temperature change after an injection of cold normal saline into one of the PAC ports at the SVC/right atrial junction. As saline injection warms in the body, the change in temperature is then measured down-stream by a thermistor. If the blood is constantly moving through the heart, then the faster the blood moves (ie, the higher the CO), the less the temperature will have decreased by the time the blood passes by the thermistor and vice versa.38 The Stewart-Hamilton equation equates the temperature

change (or lack thereof) to CO. Today’s PAC uses a heated coil and the same principles of thermal dilution to continuously monitor CO in real time rather than rely on an operator to inject saline.40 This automation of the CO measurement reduces the chance of operator error.

Another important advancement came from Martyn and colleagues41 in 1981, with the introduction of a “volumetric” PAC capable of providing information pertaining to the right

Table 1. Indications for Pulmonary Artery Catheter

AMI with suspected mechanical complications (ie, ventricular free wall rupture)17

AMI with progressive hypotension17

Acute right ventricular failure18

Severe burn patients27

Intraoperative/perioperative care Vascular surgery19

Cardiac surgery20-23

Moderate/high-risk surgical patients receiving goal-directed resuscitation16,24,25

Undifferentiated shock, not responsive to resuscitation13,26

Differentiating pulmonary from cardiac causes of pulmonary pathophysiology27

AMI, acute myocardial infarction.

Table 2. Standard Values of Hemodynamics

Variable Standard Values

Heart rate, beats/min 60–100Systolic blood pressure, mm Hg 100–140Diastolic blood pressure, mm Hg 60–90Mean arterial pressure, mm Hg 70–105Central venous pressure, mm Hg 0–8Right ventricular systolic pressure, mm Hg 15–30Right ventricular diastolic pressure, mm Hg 0–8Pulmonary artery systolic pressure, mm Hg 15–30Pulmonary artery diastolic pressure, mm Hg 4–12Mean pulmonary artery pressure, mm Hg 9–16Pulmonary artery occlusion pressure, mm Hg 6–12Cardiac output, L/min 4–8Cardiac index, L/min/m2 2.5–4.5Right ventricular ejection fraction, % 40–60Right ventricular end-diastolic volume index, mL/m2

60–100

Mixed venous oxygen saturation, % 60–80

Figure 3. Schematic of the wedge position necessary within the pulmonary artery to attain pulmonary artery occlusion pressure (PAOP) tracing. AO, aorta; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; PA, pulmonary artery; PV, pulmonary vein; RA, right atrium; RV, right ventricle; SVC, superior vena cava.





heart (right ventricular ejection fraction [RVEF], right ventric-ular end-diastolic volume [RVEDV], and right ventricular end-diastolic volume index [RVEDVI]). The principles of thermal dilution remained but were now measured at the level of the right heart only. These variables were found to be superior to the PAOP in the determination of fluid responsiveness.41-44 Nearly all catheters in place today are volumetric.

Mixed venous oxygen saturation (SvO2) is yet another

parameter available to the clinician using a PAC. The fiber-optic spectrophotometric assessment of SvO

2 in real time

became available on the PAC in the 1980s.45-47 This is a mea-sure of tissue oxygen extraction as blood transits the arteriove-nous circuit. In states of impaired oxygen delivery (ie, shock, sepsis, acidosis), tissues extract a higher percentage of oxygen than in normal states, and the SvO

2 downtrends. EN in the set-

ting of impaired oxygen delivery increases hepatosplanchic blood flow and intestinal energy demands. This phenomenon can lead to oxygen supply/demand mismatch. In extreme cases, this can lead to bowel necrosis.48 Conversely, a trickle amount of EN may induce some diversion of blood flow to the splanchic circulation and therefore provide a degree of protec-tion to the intestine. Where the tipping point between protec-tion and necrosis occurs is usually not clear in critically ill patients. It also cannot be absolutely determined by hemody-namic monitoring, laboratory assessments, or clinical exam. This is the main reason why some practitioners avoid EN in acute critical illness.

Although its popularity has waned in recent times, the information gleaned from the use of the PAC remains an important concept and tool for the critical care physician. The advent of less invasive means of hemodynamic monitoring such as arterial pulse-wave analysis and ultrasonography has shifted clinical ICU care away from the PAC. However, until prospective randomized trials have validated these newer tech-nologies, the PAC remains the gold standard for the assess-ment of hemodynamics in the critically ill patient.

Arterial Pulse-Wave Analysis in Hemodynamic Monitoring

For years now, the PAC has been the gold standard49 in acquir-ing dynamic cardiovascular performance parameters. Nonetheless, data on justifying the risk-to-benefit ratio while using this catheter have been variable, with meta-analyses sometimes suggesting measureable benefit50,51 and sometimes not.52 The question still remains in those who did not show a benefit as to whether appropriate and timely interventions were pursued in response to the acquired data.52 Ideally, the clinician should have access to a completely accurate, minute-to-minute assessment of preload, afterload, and cardiac output from which to make decisions on the role and degree of fluid resuscitation, diuresis, inotropic support, and other interven-tions. Among the list of proposed and implemented answers to the search for ideal hemodynamic monitoring modalities has been the development of arterial pulse-wave analysis (APWA).

APWA is used to estimate intravascular volume status through the use of stroke volume variation and an estimate of cardiac output. The technique is limited to patients who are on the ventilator.53 Because the data are obtained through an exist-ing peripheral arterial line that routinely exists in ventilated ICU patients, it has the appeal of little or no additional morbid-ity to the patient. For the nutrition support practitioner, the key variables of interest with APWA technology are CI and stroke volume variability. Favorable physiology is suggested by a CI of at least 2.8 L/min/m2 coupled with a trend showing improve-ment or stability at this output level. Stroke volume variability (SVV) correlates with the predicted response to volume resus-citation. Therefore, a low SVV (ie, <13 for Vigileo and <10 for LiDCO) suggests that additional fluid administration will unlikely result in significant improvement in perfusion. In our opinion, the combination of an adequate CI and a low SVV often suggests that resuscitation has progressed to a point where nutrition support might be initiated or advanced.

Similar objective hemodynamic monitoring studies assess-ing this technology are lacking, including studies looking at the limited utility in cases of arrhythmias such as atrial fibrilla-tion, the inability to correct for factors affecting arterial com-pliance such as advanced atherosclerosis, and loss of accuracy following administration of vasoactive medications such as pressors and anesthetics. In addition, stroke volume variation has only been validated as a reliable predictor of fluid respon-siveness in patients with a tidal volume between 8 and 15 mL/kg. Extremes of tidal volume, such as high-frequency oscillat-ing ventilation or severely reduced chest compliance from prone positioning, remain unproven.54

Typically, cardiac output is calculated from the product of heart rate and stroke volume of the heart. APWA substitutes pulse rate for heart rate in an effort to account for only heart-beats that actually contribute to flow away from the heart. Stroke volume, for the purposes of calculating a cardiac

Figure 4. Schematic pulmonary artery occlusion pressure (PAOP) tracing. PAOP measurement should be taken at end expiration, which is represented by point A in an intubated patient and point B in a spontaneously breathing patient.





output, is then calculated from a computer algorithm partially derived from the arterial pressure waveform. In theory, how-ever, this can only be achieved if both the systemic vascular resistance (SVR) and the systemic arterial compliance are either known or able to be closely estimated.

Historically, there have been 3 manufacturers of commer-cially available arterial waveform analysis devices. These include Pulsion (Munich, Germany), which makes the PiCCO monitoring system; Edwards Lifesciences (Irvine, CA), which makes the FloTrac sensor for use with the Vigileo monitor; and LiDCO (Cambridge, UK), which makes the LiDCO system. Each company has established and propagated a somewhat unique application of the existing theories and clinical applica-tions of APWA. Specifically, these differences have been related to the method of determining estimated systemic vas-cular resistance and arterial compliance to approximate the stroke volume necessary to calculate cardiac output. As a result, the products of each company have been shown to have characteristic advantages and disadvantages under different clinical circumstances. Most recently, each of the 3 companies has developed additional products that make use of concepts advanced by the other companies to compensate for their spe-cific product’s historical shortcomings.55

The PiCCO system measures cardiac output using pulse contour analysis and transpulmonary thermodilution. The ther-modilution is necessary for calibration. It requires a relatively central arterial access (femoral, axillary, or brachial artery) as well as central venous access. The necessity for this level of additional invasiveness has been its greatest drawback. However, there may be a reliability and accuracy advantage over uncalibrated pulse-wave analysis in terms of following CI trends in septic patients undergoing active volume expansion and/or titration of norepinephrine,56 which are common in the ICU patient population.

The FloTrac/Vigileo system is an uncalibrated system that requires only peripheral arterial access. Because peripheral arterial lines are nearly ubiquitous in many ventilated patients, the lack of necessity for any further invasive catheter place-ment, the lack of any calibration even during setup, and the ease of setup are its major advantages. Precision under circum-stances of high-dose vasopressor therapy, however, likely remains an issue despite multiple revisions to the software algorithm designed to improve this.57

In addition, because the FloTrac is uncalibrated, the com-puter algorithm alone must provide the necessary data by cal-culating a standard deviation of the measured arterial pulse pressure around the calculated mean arterial pressure over 20 seconds at 100 times per minute, generating 2000 data points from which to make the calculation. First, the computer com-pensates for previously determined characteristics of large arterial vessel compliance in humans,58-60 assesses 2 waveform features known as skewness and kurtosis, and then incorpo-rates the mean arterial pressure, the pulse rate, and demo-graphic data, including, height, weight, age, and gender, into

its calculation. The computer then continuously assesses the impact of predicted vascular tone effects on the pressure wave-form every 60 seconds and arrives at a conversion factor known as “khi.” This factor is then multiplied by the standard deviation of the pulse pressure, converting its units from mm Hg into mL/heartbeat, which effectively represents the stroke volume.61 The new calculated stroke volume is then recom-pared to the pulse waveform over the last 60 seconds to arrive at a stroke volume variation. This calculated variation has been shown to correlate with ventricular preload and volume.

The LiDCO system, like the PiCCO system, is calibrated and uses intravenous (IV) lithium reported to be in doses asso-ciated with irrelevant pharmacologic effects. Lithium indicator dilution is used by injecting lithium into a peripheral vein to calibrate the system, indirectly acquire continuous stroke vol-ume and stroke volume variation values using a root mean square mathematical model, and then finally calculate cardiac output. From an access standpoint, a peripheral arterial cathe-ter and IV are all that is necessary. Recalibration is recom-mended every 8 hours and should be done after each major hemodynamic change, which can be frequent and labor inten-sive in the hemodynamically unstable patient.62

In assessing efficacy of APWA, most reviewed studies make comparisons to transesophageal echocardiography or transpulmonary thermodilution with a pulmonary artery cath-eter. Evidence suggests that these techniques are comparable, as demonstrated by a strong correlation in measuring cardiac indices.63 Some evidence suggests, however, that transpulmo-nary thermodilution can generate clinically important time delays in the response of the PAC during rapid alterations in hemodynamic status.64 Such delays are not usually seen with pulse-wave technology, and so a discrepancy may be the result of the PAC time delay rather than inaccuracy of the APWA.

It should be noted that a number of the validation studies have been performed using one form of APWA or another. It is unclear as to whether the same conclusion might or might not be drawn about the other 2 waveform devices. Further studies involving head-to-head comparisons of the different devices would be necessary to draw such conclusions definitively.

The manufacturer of the FloTrac/Vigileo system has recog-nized certain limitations and recommends usage only in adults without ventricular assist devices or intra-aortic balloon pumps. In addition, aortic insufficiency and severe peripheral constriction during shock states or hypothermia may nega-tively affect numeric results, particularly if the arterial wave-form is measured at the radial artery in the wrist, where these effects can be most profound.61

Liu et al65 prospectively evaluated cardiac surgery patients using PACs, echocardiography, and uncalibrated APWA. Exclusion criteria included atrial fibrillation, severe arrhyth-mias, ejection fractions <35%, a permanent pacemaker, and the need for any type of mechanical cardiac support. Ultimately, 100 patients were included. PACs measured continuous car-diac output (continuous cardiac output via a thermodilutional





method) and pulmonary capillary wedge pressure (PCWP). The FloTrac sensor and Vigileo uncalibrated APWA equip-ment measured arterial pulse-wave generated cardiac output (APCO) and SVV. Transesophageal echocardiography (Sonos 5500, Philips. Andover, MA) measured left ventricular end-diastolic area and volume (LVEDA and LVEDV). APWA mea-surements were also separately made from peripheral arterial lines and central arterial lines to see if there was a difference. The authors found a tight correlation between central and peripheral APWA measurements, concluding central arterial access to be unnecessary. SVV was found to correlate well with LVEDA and LVEDV and was thus determined to be a good indicator of cardiac preload. Finally, the arterial pulse-wave estimated cardiac output was tightly correlated with con-tinuous cardiac output from the PAC.

Cannesson et al66 prospectively compared the FloTrac device with standard cardiac output measurements using the bolus thermodilution technique with a PAC in 11 patients undergoing coronary artery bypass graft (CABG). They per-formed iatrogenic volume expansion and looked for correla-tion between the PAC CO and FloTrac CO measurements. They found a good relationship between percent changes of CO after volume expansion but did not give any vasoactive medications. They validated the uncalibrated APWA model in this setting.

Lorsomradee et al67 compared uncalibrated arterial pulse contour analysis versus continuous thermodilution cardiac out-put monitoring with a PAC. This was a prospective study with 52 patients undergoing elective heart surgery. The authors found an acceptably low bias in patients without significant valve pathology. However, they recognized an unacceptable discordance during the presence of an intra-aortic balloon pump and after experimentally induced changes in arterial pressure waveform morphology seen right after the intraopera-tive sympathetic response associated with the median sternot-omy and also following phenylephrine administration. They concluded that good waveform fidelity is mandatory in obtain-ing accurate values from arterial pulse contour analysis. The use of an intra-aortic balloon pump in this study caused severe problems with measurements.

In multiple places in the literature, one finds evidence that there have been shortcomings in the software program that performs the waveform analysis in the uncalibrated model. Sequential improvements have been made to the software and its algorithms, but whether we have reached the ceiling of maximal accuracy and precision remains to be seen. Meng et al68 monitored 33 patients with the third-generation uncali-brated software and used esophageal Doppler as a control. They concluded that the Vigileo accurately tracks changes in CO when preload changes, but this accuracy is lost when the patients are exposed to vasopressors.

Other conclusions reached by various authors regarding uncalibrated pulse-wave technology have been varied. Biais et al69 determined that the Vigileo system may be used as a

predictor of fluid responsiveness in patients with circulatory failure after liver transplantation. Benes et al70 determined that fluid optimization guided by SVV during major abdominal surgery is associated with better intraoperative hemodynamic stability, a decrease in serum lactate at the end of surgery, and a lower incidence of postoperative organ complications. In another study, Biais et al71 looked at liver transplant patients with acute lung injury and ARDS on higher levels of positive end-expiratory pressure (PEEP) using the FloTrac system. They concluded that SVV is useful to predict a drop in stroke volume induced by PEEP and that the device was able to track changes in stroke volume induced by PEEP.72

Looking at the calibrated forms of APWA, some validation in the clinical scenario of reduced cardiac function exists for the Pulsion PiCCO system. Reuter et al73 prospectively evaluated 15 mechanically ventilated patients with ejection fractions under 35% after CABG surgery. Volume loading was per-formed with serial measurements of stroke volume index (SVI) until there was <5% rise in SVI with subsequent volume admin-istration. The results enabled them to conclude that stroke vol-ume variation with APWA using the PiCCO can predict volume responsiveness, and it can do so even in cases of reduced left ventricular function. Rodig et al74 compared both the PiCCO system and continuous thermodilution with the traditional intermittent transpulmonary thermodilution technique in 26 patients with CABG. They found that intraoperatively, the PiCCO generated comparable data to the continuous cardiac output catheter and that both correlated well to the intermittent thermodilution values. However, under circumstances of marked changes in SVR, an increase in the rate of recalibration became necessary to maintain accuracy. On the basis of their findings, they concluded that the PiCCO needs to be recali-brated at least once an hour and after any fluid challenges or alterations in vasoactive medication dosing.

One study comparing calibrated with uncalibrated APWA using the FloTrac and the PiCCO system should be noted. Monnet et al56 prospectively administered fluid or gave norepi-nephrine strategically in 80 ICU patients with sepsis and mea-sured cardiac indices using both systems, comparing them with transpulmonary thermodilution as a control. They con-cluded from their data that the calibrated PiCCO device was accurate but that the uncalibrated Vigileo poorly tracked the trends in CI induced by the changes in fluid administration and vasoconstrictor medication. It seemed that the more the SVR changed, the less accurate the uncalibrated data became.

Evidence exists for the benefit in obtaining dynamic data such as CO and SVV as opposed to static physiologic param-eters such as CVP, pulmonary arterial occlusion pressure, heart rate, and blood pressure for purposes of predicting fluid responsiveness and cardiac preload, as well as directing appro-priate therapy.75 Improved outcomes, at least in the case of car-diac and general surgery so far, have been demonstrated in the literature.76 Although there remains a wide variety of circum-stances under which arterial pulse-wave analysis data are





problematic,77 there does appear to be a legitimate role for the technology in the care of the critically ill. As with many newer technologies, it is not uncommon to see favorable results ini-tially that are tempered over time as clinical experience accu-mulates and more objective clinical trials are performed.

Ultrasonography

Ultrasonography is increasingly being used as a quick and noninvasive measurement tool in the ICU. In a critically ill patient, it can give immediate information on the cardiac func-tion and volume status with minimal setup time and image optimization. It is an assessment tool rather than a continuous monitoring tool that is unlike the invasive catheter methods. It requires an ultrasonography/echocardiography skill set by trained intensivists.

The gold standard for ultrasonography of the heart and great vessels has been a formal transthoracic or transesopha-geal echocardiography performed by an experienced techni-cian and interpreted by a cardiologist, but this service is often not available around the clock. The traditional model of con-sult, data acquisition, interpretation of the images, and report-ing can take over 24 hours to complete the cycle, which is too long for critically ill patients to wait.

The standard views that are obtained are as follows: para-sternal long axis, parasternal short axis, apical four-chamber, and subxiphoid views. The subxiphoid view also allows assessment of the inferior vena cava (IVC). The vena cava and its diameter change/decrease with respirations is the most reli-able test for volume status. An IVC change/decrease >80% is compatible with the need for preload volume expansion, and an IVC change/decrease <20% suggests that volume expan-sion will likely not be necessary (see Table 3). An intermediate change/decrease is indeterminate as to the need for volume expansion. This provides the role for a passive bolus, in which the legs of the patient are raised (equating to a 500-mL bolus) and the IVC collapsibility is remeasured. Decreased compress-ibility suggests that an additional fluid bolus would be benefi-cial.78 Feissel et al79 used a distensibility index of the IVC ((IVC maximum diameter – IVC minimum diameter)/IVC mean diameter) with a cutoff value of 12%. A value >12% showed that volume loading would increase cardiac output by ≥15%.

In a surgical ICU population, bedside ultrasonography has been used to assess the volume status of patients focusing on the correlations between IVC change/decrease and concurrent CVP measurements. In a study of 83 sequential patients with both the ability to obtain ultrasound measurements and CVP pressures, there was a statistically significant decrease in mean CVP as patients were in 3 ranges (change/decrease >80%, 20%–80%, or <20%).80 However, in the group with the least compressibility of the IVC (<20%), only 5% of patients had a corresponding CVP <7, and 40% of patients in this category had a CVP >7. In the group with the most compressibility of

the IVC (>60%), 60% of patients had a CVP <7, strongly sug-gesting the need for fluid expansion by both ultrasound and CVP measurement criteria. This study was unable to determine which method was more accurate or whether volume expan-sion administered for the ultrasound and/or the CVP findings improved the clinical status of the patient or outcome.

In a limited study of 30 trauma patients with hemorrhagic shock, ultrasound examination to evaluate IVC change/decrease was correlated with response to fluid resuscitation and recurrence of shock.81 In this study, the diameter of the IVC was a better predictor of recurrence of shock and a favor-able response to volume expansion than the standard vital signs of blood pressure and heart rate or base deficit decrease. This study also found a statistically significant (P < .01) cor-relation between the ultrasound diameter measurement with a computed tomography (CT) scan in those patients undergoing abdominal CT. This study suggests that bedside ultrasound can be used to diagnose hypovolemia, and acting on this informa-tion and providing volume resuscitation to the patient improved clinical outcome.

In a study of 53 trauma ICU patients, bedside ultrasonogra-phy was performed to evaluate cardiac function and IVC diam-eter measurements, with 80% of patients having an ejection fraction and/or IVC change/decrease estimated.82 Of those evaluated for cardiac function, 56% were diagnosed with left heart failure and 25% with right heart failure. Eighty percent showed respiratory variation of the IVC suggesting hypovole-mia. In a survey of how the ultrasound results were used, 87% found the ultrasound findings helpful, and 54% led directly to a change in the management plan.

Ultrasonography at the bedside in the ICU is an operator-dependent hemodynamic assessment methodology that can answer key hemodynamic questions quickly and noninvasively in real time. It has not been shown to be an effective hemody-namic monitoring technology, nor has its effectiveness been assessed by randomized clinical trials. Ultrasonography does appear to work as a complementary technology to invasive con-tinuous cardiac output catheter monitors. Ultrasonography can answer key questions intermittently, and the invasive catheters can be used to confirm the patient’s response to therapeutic interventions and to observe for future downturns in a patient’s hemodynamic status. ICU-performed ultrasonography results

Table 3. Respiratory Variation With the IVC Diameter and Correlation With CVP Estimation83

IVCCVP Estimate,

mm Hg

Diameter <20 mm and >50% inspiratory collapse ≤5Diameter <20 mm and <50% inspiratory collapse 10Diameter >20 mm and <50% inspiratory collapse 15Diameter >20 mm and no inspiratory collapse 20

CVP, central venous pressure; IVC, inferior vena cava.





are often not directly recorded as an isolated study in the medi-cal record. The result is more typically documented in the ICU note. Therefore, direct communication with the intensive care practitioner performing ultrasonography and directly caring for the ICU patient is necessary. In our opinion, if the results of ultrasonography show an acceptable cardiac output and a low degree of compressibility of the IVC, then adequate perfusion is usually present, and the recommendation to initiate or advance nutrition support can frequently be made.

Summary

A major challenge in critical care medicine remains the need to predict optimal resuscitation parameters for each patient given his or her unique physiology coupled with the dynamic effects of the patient’s illnesses. Hemodynamic monitoring and directing the resuscitation of the patient based on data collected from these devices remains a staple of critical care. Which devices, whether to use them individually or collec-tively, and how to best use them to optimize outcomes remain a major challenge in the evidence-based medicine approach to critical illness and shock.1,74,81 It is important to emphasize that despite the potential for guidance by collect-ing hemodynamic measurements as described above, the final judgment as to whether adequate perfusion exists to justify the initiation or advancement of nutrition support should be determined by the critical care team and should be primarily based on the patient’s response to therapeutic inter-ventions over time.

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Hemodynamic Monitoring in the Intensive Care Unit