Hello, and welcome to this presentation on cardiac output monitoring devices as part of the multi-professional critical care review course for adult critical care. My name is David Kaufman. You can see my email address there if you have questions or queries or concerns that you wish to share. I'm on the faculty of the NYU School of Medicine in New York City, where I work at the University Hospital as part of the Division of Pulmonary and Critical Care Medicine. And I'm going to talk today on hemodynamic monitoring, the use of bedside measurement of cardiovascular physiology. I have some conflicts of interest to disclose. I have received grant funding and travel reimbursements from the company Cheetah Medical, which is now part of Baxter. And I work as a member of the Medical Advisory Board for Pulsion Medical Systems, which is now a part of Yetinga. And Pulsion has also paid for travel arrangements as well as speaking honoraria. I just want to stipulate that any figures that I use are to illustrate only, and they're not intended to advocate for the use of a specific product or class of products. Also, this is not a comprehensive list of all technologies that may be available, just the ones that are most commonly encountered. Funding objectives for this presentation are to give a short explanation of what exactly is monitoring, to talk about what some of the goals of monitoring are, especially cardiovascular monitoring in the critical care setting. We're going to discuss what kinds of monitors are commonly available for achieving these goals. And then we're going to talk a little bit about what kinds of clinical questions can we answer with these monitors. What is monitoring? Well, ICU monitoring is a really big topic. There is a textbook. You can see its dimensions there. It's 1,560 pages and it weighs about 8.4 pounds, so it functions really well as a doorstop. And it's available in used editions. You can see some of the recent prices there if you really want to take a deep, deep dive into this topic. But we're going to take a sort of shallow dive into the topic. And we're going to talk a little bit about what monitoring is exactly in a relatively basic sense. Our term monitor, when it's used as a transitive verb, is derived from the classical Latin monitor, who is a person who suggests or advises. And it's derived from the past participle of the Latin verb monere, to warn or to remind. It was first used in English as a verb almost 200 years ago with the meaning to guide as a monitor. And it started to have its current meaning, which is to check or regulate the technical quality of a transmission without causing interruption or disturbance nearly 100 years ago. And it became associated with using things like radar or sonar or other kinds of technology with the purpose of regulation or control during World War II. A crucial thing to keep in mind about monitoring is that no monitoring device or technique, no matter how accurate or insightful, will, in and of itself, improve patient outcomes. In order for a monitor to improve patient outcomes, it has to be coupled with some treatments. Treatments that theoretically are guided by the monitor in order to improve patient outcomes. For practical purposes, ICU monitoring is the use of continual or very frequent measurements to detect imminent danger or response to treatment. It also could mean the data acquisition in order to try to ascertain the state of a patient who's at a high risk for worsening or to detect whether that patient is improving with the therapy that you've prescribed. Now that we've established a somewhat basic and common sense notion of what monitoring is, I'd like to discuss what are the goals of cardiovascular monitoring in the intensive care setting. Ultimately, the goal of fluid or hemodynamic management in the ICU is to support normal cellular metabolic function. We try to achieve normal cellular metabolic function by maintaining or restoring the effective coordinated function of the macrocirculation and the microcirculation, as well as trying to restore or preserve an intact cellular metabolism. Practically speaking, most clinical management that we perform to manipulate cardiovascular parameters in the ICU is currently targeted at macrocirculatory variables like cardiac output and blood pressure, as well as surrogates of cellular metabolism like the blood lactate level or the base excess. The therapeutic rationale of giving intravenous fluids to achieve these ends is to optimize macrocirculatory function with the hope of improving or optimizing microcirculatory and cellular function. In our best current theoretical framework, we believe that normal cellular function depends on adequate tissue oxygen delivery, which is governed by two factors, the arterial oxygen content, which is a blend of the hemoglobin concentration and the oxyhemoglobin saturation multiplied by 1.34, which is the amount of oxygen that can be carried on every gram of hemoglobin with a very small complement of oxygen that's dissolved in the plasma. Oxygen delivery is merely the arterial oxygen content multiplied by the cardiac output. And although our current theoretical model is somewhat powerful, it's almost certainly incomplete or inadequate. Or as the famous statistician, Dr. Box once said, all models are wrong, but some models are useful. For the purposes of hemodynamic or cardiovascular monitoring in the ICU, the best theoretical monitor that we could have would give information about cellular metabolism and why it's failing. Whether substrate delivery or substrate utilization is the center of the problem and whether substrate delivery is enough to meet the demand that the tissues have for substrate. It's important to recognize that we do not yet have this monitor. We have a lot of substitutes. We can use blood lactate levels, gastroenterometry, capillary refill time, oxygen tension in the tissues, in the mixed venous blood, in the central venous blood, or we can use sublingual capillary density measurements. But until we have better monitors, most of our current monitors are aimed at the oxygen delivery part of this equation, where we try to manipulate hemoglobin and oxygen saturation, as well as cardiac output in the form of stroke volume and heart rate. Thus, the goals of most ICU cardiovascular monitoring are to assess the ability of the cardiovascular system to deliver oxygen to the tissues and to measure the effect of the interventions whose aim is to improve oxygen delivery and tissue blood flow, usually by improving the cardiac output or arterial blood pressure. With that framework, I'd like to discuss for a little while what kinds of monitors are out there currently. The basis for the cardiac monitors that currently exist include use of the Fick principle, endocrine dilution techniques, analysis of the arterial pulse waveform, thoracic impedance or bioreactance, or taking advantage of the Doppler effect. The Fick principle was first described in 1870, and it holds that the cardiac output is equal to the oxygen utilization, the VO2, every minute, divided by the arteriovenous oxygen content different multiplied by 100. This equation can be modified for partial carbon dioxide re-breathing, where the cardiac output is equal to the difference between the volume of carbon dioxide exhaled per unit time under normal conditions and then under re-breathing conditions, divided by the arterial content of carbon dioxide under normal conditions, subtracted by the volume of carbon dioxide extracted from the arterial content of carbon dioxide under re-breathing conditions. This is performed by use of a proprietary partial re-breathing circuit that you can see pictured here. This technology, which is found on the volumetric capnograph machines manufactured by Phillips Respironics, has some advantages. It's a non-invasive, accurate, automated, easy-to-use monitor that provides nearly continuous information about the cardiac output. Some of the disadvantages are that the patient's trachea must be intubated for this monitor to be useful, and unfortunately this monitor is not very accurate in the presence of lung disease with severe gas exchange abnormality or in states where there are severe hemodynamic derangements, making the applicability of this monitor to many intensive care situations somewhat questionable. Other monitors of the cardiovascular system work on the indicator dilution technique model, which is based on the Stuart-Hamilton equation that you can see in this slide. Essentially, some kind of tracer is injected into a central vein, and then the level of that tracer is watched over several cardiac cycles to see how much of that tracer decreases over time. This is the technique that is used by the pulmonary artery catheter developed by Swan Gans in the 1960s and introduced into clinical medicine in the 1970s. Essentially, an indicator, cold fluid, is injected into the superior vena cava, and then there's a thermistor on the pulmonary artery that helps detect temperature change as this cold bolus moves through the circulation. And here, the readout for cardiac output is the right ventricular output. A similar technology is used by the PICO or volume-use systems in which a cold fluid is injected into the superior vena cava, but here the thermistor is on a catheter in a central artery such as the femoral or axillary artery. Here the cardiac output is equal to the left ventricular stroke volume. Pulse dye densitometry utilizes an intravenous dye injection and then a colorimetric sensor on the fingertip. And lithium dilution uses a bolus of lithium that's injected either into a central or peripheral vein and then measured by a sensor that's on an indwelling peripheral arterial catheter. Some of the characteristics of these devices include that most pulmonary artery catheters give you intermittent values for stroke volume and cardiac output. There are some pulmonary artery catheters that can give you a continuous cardiac output, but they're more expensive and are not used quite so much as the standard pulmonary artery catheters. Pulse dye densitometry is intermittent and can be done maybe only a few times an hour. Pulmonary thermodilution gives an initial calibration and so does lithium dilution where the cold injectate or the lithium injectate is used first to calibrate the device and then arterial waveform analysis is used to give continuous hemodynamic parameters. This cartoon shows the injection of lithium into the central vein and then you can see the black sensor hooked up to the arterial catheter tubing in figure two where the lithium concentration in the peripheral artery is measured, which gives a display on the monitor, which is then transformed into a measurement of cardiac output. Edwards VolumeView and Pulsions PicoSystems work on essentially the same principle as each other. Both of them involve, like I said before, the injection of cold saline or cold fluid into the superior vena cava with detection on an arterial catheter with a thermistor that will measure the temperature rising and falling in response to this injection of cold fluid. The VolumeView system is used with catheters that are inserted into the femoral artery and the PicoSystem uses catheters that can be inserted into the axillary, brachial or femoral arteries. The pulse waveform can be analyzed to give information about cardiac output or stroke volume. In devices such as Lidco Plus, VolumeView, or Pico, the pulse waveform device is first calibrated with the use either of a lithium or cold saline injection and then further analysis on a beat-to-beat basis of the arterial waveform gives you beat-to-beat stroke volume and cardiac output information. Uncalibrated devices that analyze the pulse waveform include the Lidco Rapid device, the FlowTrack device, the ProAQT device, the ClearSight device, which is marketed by Edwards and used to be marketed by a company called B-Mine, the CNAP application, which is marketed by Lidco as CNAP, or NICCI by the Pulsion Company. All of these techniques look at the characteristics of the time pulse waveform on an arterial catheter, looking at the systolic area, that is the area under the curve prior to the dichrotic notch, and the diastolic area, which is the area under the curve after the diastolic arch. And then it looks at the area to make certain calculations about preload, contractility, and afterload. As I've mentioned, in calibrated devices such as VolumeView, Pico, or Lidco+, an indicator is initially injected to calibrate the device, and then beat-to-beat information about stroke volume and cardiac output is provided by waveform analysis that is performed at the same time as the initial indicator dilution test. Periodic recalibration is required to make sure that the waveform analysis remains accurate when it represents the stroke volume and cardiac output. Uncalibrated devices take patient information, such as demographics, comorbidities, and the kinds of medications the patients are receiving, and then puts those pieces of information into an algorithm that's used to estimate aortic impedance and compliance, as well as peripheral arterial resistance, to give a value for stroke volume and cardiac output. Immediately, though, you can see where error might creep into these measurements, because when patients are on vasopressors or have valvular heart disease or other kinds of cardiovascular abnormalities, it's hard to account for all of these characteristics in the algorithm, thereby throwing off the accuracy of the stroke volume measurement. This picture shows some of the devices that are available for pulse waveform analysis and cardiac output monitoring. You see in the first two images, the top two images, you see the PICO catheter and the Edwards Volume View catheter, which can be inserted into the femoral artery, although the PICO catheter can also be inserted into an axillary or brachial artery. Below you see the sensors, the Pulsion Proact and the Edwards FlowTrack sensors, which can be placed in line with a standard arterial catheter in order to give stroke volume and cardiac output information. And then you see two different devices, the CNAP-CNS systems and the ClearSight system, which use analysis of the pulse waveform in the fingers to give information about the stroke volume and cardiac output. Some of the advantages associated with the calibrated devices is that they are very, very accurate compared to the gold standard, which is pulmonary artery catheterization. They give lots of information besides just stroke volume and cardiac output, and they are continuous. The disadvantages of these systems is that they require a catheter be placed in a central artery and that they require periodic recalibration to remain accurate. Uncalibrated sensors have the advantages of being able to use a standard arterial catheter and good linearity. That is to say that tracking over time with these stroke volume cardiac output devices tends to track with the changes in the true value. They're also continuous. However, a big disadvantage of these systems is that their accuracy in giving an absolute number for the stroke volume of cardiac output is sometimes inaccurate, especially in many relevant clinical situations, such as valvular heart disease, the use of large doses of vasopressors, and so forth. Some of the additional information that comes off of the calibrated central arterial catheters that use cold thermodilution through a central arterial line, like the PICO device or the volume view device, is they give lots of additional information based on the decay characteristics of the curve, the decay curve characteristics of the injected thermal indicator. For example, the derivative of that slope is a measure of the thermal loss of fluid to the tissue outside the vasculature, which is used to estimate the amount of extravascular fluid, giving you a measure of extravascular lung water. Several technologies exist to try to give non-invasive or minimally invasive readings of stroke volume and cardiac output based either on bioimpedance or bioreactance or ultrasound technologies. These devices include the Cheetah Starling SV or the Bio-Z, the Deltex CardioQ, USCOM, or just the use of standard bedside ultrasonography. Bioimpedance and bioreactance are non-invasive measurements of stroke volume and cardiac output. These technologies use electrodes that are placed on the skin. These electrodes emit and absorb a high frequency but low voltage of electrical signals and compares the impedance characteristic at four points on the patient during cardiac cycles and makes a relationship between those impedance changes and aortic blood flow. Thus, these monitors are able to estimate the aortic blood flow, that is the stroke volume, based on derivatives of the impedance changes. The Cheetah Starling SV system uses bioreactance, which incorporates phase shifts related to the electrical properties of blood to achieve higher accuracy. Some of the advantages of these kinds of systems include that they are non-invasive, provide continuous information, and show good linearity. Some of the disadvantages include questionable accuracy and a large variety of sources of error, including motion, such as respiratory efforts, or electrical interference from other equipment that may be in the ICU. Several ultrasound-based devices are able to give information about stroke volume and cardiac output. The Deltex CardioQ device is an esophageal probe that sits in the esophagus adjacent to the thoracic aorta and is able to measure aortic blood flow using a Doppler signal. The USCOM device works on a similar principle, but here the probe is placed in the suprasternal notch and aimed towards the aortic arch and thereby detect aortic blood flow using a Doppler signal. Standard bedside ultrasound technique can measure the velocity-time integral in the left ventricular outflow tract to come up with an estimate of stroke volume as well. Here I've listed some of the advantages and disadvantages of these technologies. Many of them are continuous and provide good linearity. One of the benefits of the ultrasound in particular is that it utilizes already existing equipment and is non-invasive. But the disadvantages are considerable. For example, they have questionable accuracy with the true value of stroke volume and cardiac output and all of them are highly positionally dependent. That is, two different users or even the same user at different time points may be measuring aortic blood flow or a left ventricular outflow tract blood flow from slightly different angles introducing error into the estimate of stroke volume. A lot of practitioners show a great deal of enthusiasm about using ultrasound to look at the inferior vena cava and draw some conclusions about cardiac performance. It's really, really important to keep in mind that this is not a measurement of cardiac output and it is actually an attempt to answer a different but related question. And that's a pretty good segue into what are the kinds of questions, physiological and clinical that we can try to answer with the current crop of monitors. Is it enough to know stroke volume and cardiac output? And if it's not enough, what additional information can help us? This figure is called the Bellamy curve after the author of an editorial and I think it was the British Journal of Anesthesia some 20 years ago. This editorial posits that there's a U-shaped curve of intravenous volume that describes the relationship of intravenous volume and the risk for morbidity and mortality. You can see that there's an optimal point in the U-shaped curve where morbidity and mortality are minimized, but that either hypovolemia or fluid overload can be associated with an increased risk for complications. As we've said before, most of the monitoring systems that we used are aimed at looking at the cardiac output and more specifically the stroke volume aspect of the oxygen delivery equation. What most of these monitors are able to do is help us describe the Frank-Starling curve on which our patient might find herself. That is, is the patient on a flat, failing heart Frank-Starling curve where increases in stroke volume are unlikely to occur as we increase preload? Or does the patient's heart have a relatively normal Frank-Starling curve? If so, at what part of the Frank-Starling curve does the patient find herself? Therefore, by increasing preload, do we increase stroke volume? It also helps us answer the question, if the patient is on the failing heart curve, can we move that patient to a normal or even supraphysiologic heart curve by using chemical or mechanical inotropes? What the current crop of most ICU hemodynamic monitors can do is allow us to take advantage of what we call functional hemodynamic monitoring. Functional hemodynamic monitoring describes the use of following changes in stroke volume and cardiac output that occur naturally under the conditions of positive pressure ventilation to come up with some estimate of how the cardiovascular system is going to react when presented with more preload, more afterload, or more inotropy. You can see some of the phenomena of heart-lung interactions described in this slide. One phenomenon that we can use to understand how the cardiovascular system is going to react is called pulse pressure variation. The pulse pressure variation describes the maximal difference in the arterial pulse pressure between end inspiration and end expiration. A pulse pressure variation of greater than 13% accurately predicts volume responsiveness in a broad variety of ICU patients. Stroke volume variation uses a similar principle. Here, instead of measuring the difference between the pulse pressures, the algorithms in the pulse waveform analysis devices can rapidly integrate the systolic portion of the pulse waveform to estimate the stroke volume. When the stroke volume variation is greater than 10% between inspiration and expiration, it highly accurately predicts whether a patient will improve the cardiac output or stroke volume with additional fluid loading. A related phenomenon is the passive leg raise maneuver. This uses a similar principle in which following the stroke volume and cardiac output as the body's own reservoir of approximately 500 milliliters of whole blood that's stored in the lower extremity venous circulation will improve stroke volume and cardiac output when that volume of blood is transferred to the central veins. Functional hemodynamic monitoring has substantial limitations. For example, in order to be able to use pulse pressure variation or stroke volume variation, all patients must be on positive pressure ventilation and they must not be triggering any spontaneous breaths. The patients must be basically in normal sinus rhythm. They can't have any atrial arrhythmias and it's difficult to do these calculations unless you have a printout of the pulse waveform or use one of the marketed devices that does it automatically. Passive leg raising overcomes many of these limitations. That is, you can use them when a patient is not on positive pressure ventilation, when a patient is spontaneously breathing, or in the presence of atrial arrhythmias. You still have to have a continual measurement of stroke volume and cardiac output and you have to be aware that the passive leg raise maneuver will not work as well in patients who have high intra-abdominal pressure. Targeted measurements include measuring the stroke volume at end expiration and end inspiration, doing a tidal volume challenge, that is, suddenly increasing the tidal volume, or doing a PEEP challenge, that is, doing a sudden increase in PEEP and measuring the changes in stroke volume and cardiac output. As we've discussed briefly, looking at the inferior vena cava with an ultrasound can potentially be helpful in assessing fluid responsiveness. Again, this is in theory. This can only really be done accurately when the patient is ventilated with positive pressure ventilation and is not making any spontaneous respiratory efforts. Furthermore, there's not a lot of data that backs up using this index as a marker of fluid responsiveness. Looking at the IVC is not a continuous monitor and it's subject to multiple sources of error. In a very good review that Dr. Millington wrote a couple of years ago, ultrasound assessment of the inferior vena cava appears easy and fun, but it may not be as helpful as we hope. A very, very, very important limitation of all of this is that the presence of fluid responsiveness does not mean that fluid will be beneficial. There are several reasons why this might be the case. It might be that the patient shows fluid responsiveness, but that the stroke volume is actually sufficient. This is true of probably everybody listening to this presentation right now. You're probably fluid responsiveness, but you don't have cardiovascular insufficiency. Patient could be fluid responsive, but that fluid responsiveness does not yield a very large increase in stroke volume or cardiac output. Maybe it's only 10 or 15%, which may not be enough to increase oxygen delivery enough to overcome some of the shock. The patient could be fluid responsiveness and the cardiac output increases, but that cardiac output increase does not result in improved tissue perfusion due to a very bad state of the peripheral vasculature. Finally, there may be conditions in which a patient's cardiovascular system shows signs of fluid responsiveness, but even though fluid responsiveness is present, giving additional fluids might be harmful. That is, the harm outweighs any potential benefit. One such example is the extravascular lung water is rising, leading to pulmonary edema and potentially ARDS. In other words, we should be very careful when we decide to give intravenous fluid boluses. We should avoid the reflex tendency to see an elevated blood lactate and to give a bolus of fluid. As I've mentioned, some of the devices, especially VolumeView and PICO, give information about when intravenous fluids may be causing harm. Using transpulmonary thermodilution gives information about the extravascular lung water, which is a highly accurate measurement of the amount of edema that's forming in the interstitium and alveoli of the lungs. High extravascular lung water values are associated with an increased risk for developing ARDS and for dying. These signals may be very important signals that harm is accruing when we decide to give more intravenous fluid. A few years ago, a panel of experts gathered to describe the appropriate times to use some of these less invasive or invasive cardiac output monitors. You can see in the lower right corner that if a patient is developing ARDS or the patient's response to initial therapy is insufficient, transpulmonary thermodilution systems or a pulmonary artery catheter can be highly accurate and useful measurements of cardiac and cardiovascular performance that help bedside clinicians make better decisions about what interventions to perform next. Before concluding, I want to point out some helpful reading if you want to learn more about this topic. There's a very good and relatively concise chapter in the Martin Tobock textbook of mechanical ventilation that talks about ICU monitoring. Miller's anesthesia textbook also has a very good chapter on the fundamental principles of monitoring and instrumentation, as well as another chapter on cardiovascular and respiratory monitoring. The whole topic of functional hemodynamic monitoring is discussed well in the American Journal of Respiratory and Critical Care Medicine now over 15 years ago, and a recent article in the journal Perioperative Medicine discusses some of the physiology and clinical aspects of fluid management in the perioperative and critical care settings. A relatively recent article in the Annals of Cardiac Anesthesia discusses the various technologies and options available for the monitoring of cardiovascular performance in the operating areas or in the ICU. The evidence base that the use of these monitors is associated with better patient outcomes is growing. There was a meta-analysis by Bednarczyk and co-authors published in Critical Care Medicine a few years ago, which looked at goal-directed therapy that used various fluid responsiveness strategies showing that these strategies probably are associated with clinical benefit. Two relatively recent papers, one by Latham in the Journal of Critical Care and one by Douglas that's published online right now in the journal Chest, look at studies of fluid responsiveness to guide sepsis volume resuscitation and presser resuscitation, and both of these studies have found potentially significant clinical benefit associated with these strategies. And with those references, I'd like to conclude this presentation, and thank you for your attention. Good luck.

cardiac output monitoring devices

hemodynamic monitoring

Fick principle

indicator dilution techniques

arterial pulse waveform analysis

functional hemodynamic monitoring

fluid responsiveness assessment