Pulmonary Artery Catheters

" a fool with a tool is still a fool."

Chad's and My article

Fast Flush Test

when patient is in profound shock, CVP increases to match mean BP

force driving fluid from periphery to heart is the elastic recoil from distended small veins and venules; this is the mean circulatory filling pressure

Normal gradient for venous return is 4-6 mmHG

Cardiac function curves plateua at <10 in normal folks

Zeroing

Sets monitoring to zero relative to atmosphere. If ATM is 760 and CVP is 10, then it is really 770

Leveling

best would be 5cm below sternal angle

Where to measure

best at base of c wave

use base of a wave when c is not there

Use wave immediately after QRS

CVP is measured relative to ATM but does not take into account the transmural pressure of the heart (the difference between the outside and inside)

a and v waves

a wave typically larger than v wave

Great CVP article (Curr Opin Crit Care 2006;12:219)

CVP

Emerg Med J 2003; 20:467-469
Is the central venous pressure reading equally reliable if the central line is inserted via the femoral vein
yes!

Noninvasive Monitoring of Peripheral Perfusion

(Intens Care Med 2005;31:1316)

Skin temperature

NIRS
 

Radial a-lines correlated with femoral in shock patients on vasopressors (Crit Care 2006;10:R43)

(

)

Volume 34(8), August 2006, pp 2224-2227

Central venous pressure&#...Central venous pressure: A useful but not so simple measurement
[Concise Definitive Review]
Magder, Sheldon MD

Section Editor(s): Dellinger, R Phillip MD, FCCM, Section Editor

From McGill University Health Centre, Montreal, Quebec, Canada.
The author has not disclosed any potential conflicts of interest.
Abstract
Objective: To review the clinical use of central venous pressure measurements.

Data Sources: The Medline database, biographies of selected articles, and the author's personal database.

Data Synthesis: Four basic principles must be considered. Pressure measurements with fluid-filled systems are made relative to an arbitrary reference point. The pressure that is important for preload of the heart is the transmural pressure, whereas the pressure relative to atmosphere still affects other vascular beds outside the thorax. The central venous pressure is dependent upon the interaction of cardiac function and return function. There is a plateau to the cardiac function curve, and once it is reached, further volume loading will not increase cardiac output.

Conclusions: If careful attention is paid to proper measure-ment techniques, central venous pressure can be very useful clinically. However, the physiologic or pathophysiological significance of the central venous pressure should be considered only with a corresponding measurement of cardiac output or at least a surrogate measure of cardiac output.


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Central venous pressure measurements are frequently used for the assessment of cardiac preload and volume status (1). This is not surprising, considering the ready availability of central venous pressure measurements for any patient who has a central venous line. Central venous pressure can even be estimated in most people by examining the distention of jugular veins (2). However, the use of the central venous pressure is much criticized because central venous pressure poorly predicts cardiac preload and volume status (3–5). I argue that the reason for the lack of appreciation of the usefulness of the central venous pressure is the failure to consider the physiologic determinants of the central venous pressure and potential errors in measurement (6, 7).

PRINCIPLES OF MEASUREMENT
Before we assess the physiologic meaning of the central venous pressure, some basic principles of measurement need to be considered. An important point that is often not respected is that hydrostatic pressures are relative to an arbitrary reference level, and changes in the reference level change the measured pressure. The effect of leveling on the measurement of central venous pressure is particularly important because small changes in central venous pressure have large hemodynamic effects. For example, the normal gradient for venous return is in the range of 4 mm Hg to 6 mm Hg (8), and the normal cardiac function curve starts at 0 and plateaus in most people by 10 mm Hg. The commonly accepted reference level for vascular measurements is the midpoint of the right atrium, for this is where the blood returning to the heart interacts with cardiac function. As routinely taught to medical students, this can be identified on physical examination at a vertical distance 5 cm below the sternal angle, which is where the second rib meets the sternum (2). This is true whether the subject is supine or sitting up at a 60-degree angle because the right atrium is anterior in the chest and the atrium has a relatively round shape. Thus, a 5-cm vertical line from the sternal angle remains in the approximate center of the atrium even when the person is sitting upright at a 60-degree angle. This means that patients do not have to be supine for measurements when this reference level is used.

More commonly, the mid-thoracic position at the level of the fifth rib is used in intensive care units. This is easier to teach but should be used only for measurements in the supine position, because this reference position changes in relation to the mid-right atrium with changes in posture. The greater simplicity of the mid-thoracic position also likely results in less rigor in proper leveling. Values measured relative to the mid-thoracic reference level are on average 3 mm Hg greater than those based on the reference level 5 cm below the sternal angle (9).

A second important principle of measurement is that the value of central venous pressure that determines cardiac preload is the central venous pressure relative to the pressure surrounding the heart, or what is called the transmural pressure. This too is the source of a lot of measurement errors (10). The heart is surrounded by pleural pressure, and pleural pressure varies relative to atmospheric pressure during the respiratory cycle, whereas measuring devices are zeroed relative to constant atmospheric pressure. At end-expiration, pleural pressure is only slightly negative relative to atmospheric pressure, and thus the central venous pressure measured relative to atmosphere at this part of the cycle is close to the transmural pressure, whether the person is breathing spontaneously or with positive-pressure ventilation. However, in patients breathing with positive end-expiratory pressure (PEEP), transmural central venous pressure relative to atmosphere will always overestimate the transmural pressure, and there is no simple way to correct for this problem. At low levels of PEEP, however, especially in patients with decreased lung compliance, the effect is small. Furthermore, as discussed below, it is really the hemodynamic response to a change in central venous pressure that is important clinically.

Although expiration is normally passive, active expiration is very common in critically ill patients. When expiration is active, contraction of abdominal and thoracic muscles increases pleural pressure during expiration, and there may not be any phase during the respiratory cycle in which pressure measured from a transducer referenced relative to atmospheric pressure gives a close approximation of atrial transmural pressure (Fig. 1). The only thing that then can be done in this situation is to examine multiple cycles and make the measurement in a cycle where there is minimal forced expiratory effort. Sometimes, there is no value that is satisfactory, and a measurement early in the expiratory phase may be a better estimate than the value at end-expiration, but it is still a guess.



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[Help with image viewing]
[Email Jumpstart To Image] Figure 1. Example of a central venous pressure (CVP) tracing for a patient with forced expiration. Insp and the lines mark inspiration. The pressure rises throughout the expiratory phase because of transmission of pleural pressure to cardiac structures. Making the measurement an end-expiration will greatly overestimate the true central venous pressure. The digital value on the monitor will also likely be an overestimate. A reasonable guess is a measurement early in expiration, before the patient begins to push (arrow).

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Another important consideration for the measurement of central venous pressure is where to make the measurement in relation to the normal “a,” “c,” and “v” waves. The “a” and “v” waves can often be in the range of 8–10 mm Hg, which means that there is a large difference in the value at the top, middle, or bottom (Fig. 2). The choice is arbitrary and each part of the cycle has physiologic significance. However, for the estimate of cardiac preload, which is the most common clinical question, the pressure at the base of the “c” wave is most appropriate because this is the last atrial pressure before ventricular contraction and therefore the best estimate of cardiac preload (11). If the “c” wave cannot be identified, the base of the “a” wave gives a good approximation. Alternatively, if the monitor has the capacity, a vertical line drawn through the Q wave of the electrocardiogram will help identify this position. On the other hand, if there is a tall “a” or “v,” the peak of these waves still has hemodynamic consequences for upstream organs such as the liver and kidney. Furthermore, the central venous pressure in most dependent parts of the body in the supine position is 8–10 mm Hg higher than that measured on the basis of 5 cm below the sternal angle measurement, and this is the pressure that drives the local capillary filtration.



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[Help with image viewing]
[Email Jumpstart To Image] Figure 2. Example of a central venous pressure (CVP) tracing with prominent “a” and “v” waves. There is a small “c” wave after the “a” wave, followed by the “x” descent. The appropriate point for measurement is the base of the “c” wave (or the “a” wave when the “c” wave cannot be seen). In this example, the difference between the bottom (the correct position) and the top is 8 mm Hg.

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The central venous pressure can be estimated on physical examination by measuring the distention of the jugular veins relative to the sternal angle. One then adds 5 cm H2O to the measured distention to obtain the central venous pressure (12). To convert the value of central venous pressure in cm H2O to mm Hg, one needs to divide the value in cm H2O by 13.6, which is the density of mercury compared to that of water, and multiply by 10 to convert cm to mm Hg (or simply divide by 1.36). It is worthwhile doing this before inserting central lines, for the pressure estimate will tell you that the value obtained with the transducer is in the appropriate expected range. It also improves one's skills in using the jugular venous distention to assess central venous pressure noninvasively.

DETERMINANTS OF THE CENTRAL VENOUS PRESSURE
Central venous pressure is determined by the interaction of two functions: cardiac function, which represents the classic Starling length-tension relationship, and a return function, which defines the return of blood from the vascular reservoir to the heart (13). Thus the central venous pressure by itself has little meaning. The central venous pressure in a normal person in the upright posture is usually less than zero (atmospheric pressure) with a normal volume and normal cardiac function (14). However, a low central venous pressure also can indicate hypovolemia or can be present in someone who is hypervolemic (i.e., with increased return function) but has a very dynamic heart. On the other hand, a high central venous pressure can be present in someone with a high volume and normal cardiac function as well as in someone with normal volume and decreased cardiac function. Thus, a central venous pressure measurement must be interpreted in the light of a measure of cardiac output or at least a surrogate of cardiac output, such as venous oxygen saturation or pulse pressure variations. The situation is similar to the analysis of Pco2; to properly interpret the clinical meaning of Pco2, one needs to know the pH.

USE OF THE CENTRAL VENOUS PRESSURE
Central venous pressure is commonly used to optimize cardiac preload. However, an essential point is that the cardiac function curve has a plateau and when that plateau is reached, further volume loading and increasing the central venous pressure will not alter cardiac output. The increase in central venous pressure will only contribute to peripheral edema and congestion of organs. The plateau is due to restriction by the pericardium, or in the absence of the pericardium, the cardiac cytoskeleton. A difficult problem for managing the care of patients is that the central venous pressure at which cardiac filling is limited is highly variable (3, 15, 16). It can occur at a central venous pressure as low as 2 mm Hg (measured relative to 5 cm below the sternal angle) but also as high as 18 to 20 mm Hg. However, as a working number, the cardiac function curve will plateau in most people by a central venous pressure of ~10 mm Hg (12–14 mm Hg when the mid-thoracic reference level is used) (9). When the central venous pressure is higher than 10 mm Hg and there is a question of the potential for a volume load to increase cardiac output, one should first consider possible reasons for why the central venous pressure is higher than normal. Explanations include chronic pulmonary hypertension, high positive end-expiratory pressure (whether external or internal), and some other restrictive processes.

The “gold standard” for determination of whether or not cardiac function is volume-limited is to perform a fluid challenge and determine whether an increase in central venous pressure results in an increase in cardiac output. For this purpose I recommend that there be an increase in central venous pressure of at least 2 mm Hg, for that magnitude of change can be recognized on most monitors. For the test to be positive there should be an increase in cardiac output of 300 mL/min, a value in the range of reproducibility of thermodilution cardiac output devices (17). In reality, even smaller changes in central venous pressure should increase cardiac output in someone whose heart is on the ascending part of the cardiac function curve. Consider someone in whom the plateau of the cardiac function curve occurs at a central venous pressure of 10 mm Hg and the cardiac output at the plateau is 5 L/min. The slope of the line connecting the plateau to the zero intercepts indicates that cardiac output should increase by 500 mL/min for every 1-mm Hg increase in central venous pressure, and that is still an underestimate of the steep part of the function curve. Furthermore, the increase in cardiac output should occur as soon as the central venous pressure is increased, for on the basis of Starling's law, an increase in end-diastolic volume will affect the stroke volume of the next beat.

If the clinical question is simply to determine whether the person is volume-responsive at a given central venous pressure, the type of fluid used for the fluid challenge is not important. What is important is to run the fluid in as fast as possible; the faster the fluid is given, the lesser has to be given. When I am concerned about giving too much volume unnecessarily, I sometimes use a pressure bag to increase the speed of the infusion, and as soon as the central venous pressure increases by 2 mm Hg, I measure the cardiac output.

An interesting approach to a volume challenge that can avoid extrinsic volume infusion is to elevate the patient's leg to provide an autotransfusion and observe the cardiac response (18). Another possible test is to perform a hepatojugular reflux (12). In this test the abdomen is compressed and the effect on jugular venous distention is observed. It has been shown that if jugular venous distention persists for more than 10 secs, it is indicative of right-heart dysfunction, and although this has not been directly studied, it would likely mean that the patient will not respond to volume.

The important clinical question with regard to fluid responsiveness in most patients should be phrased in the negative: “Is it unlikely that this patient will respond to fluids?” To this end, examination of the pattern of respiratory variations in the central venous pressure is useful to predict a lack of fluid responsiveness in patients who have spontaneous inspiratory efforts (15). This examination was also shown to be effective for patients who are mechanically ventilated but have at least some triggered efforts. The first step is to determine whether there is an adequate inspiratory effort. If the patient has a pulmonary artery catheter in place, respiratory fluctuations in pulmonary artery pressure give an indication of the adequacy of the inspiratory effort. If there is no pulmonary artery catheter, simple observation of the patient is often adequate. If the central venous pressure as measured at the base of the “a” wave falls by >1 mm Hg during inspiration and this is not due to the relaxation of expiratory muscles, usually the patient will respond to fluids, although some patients may not. However, the test is more important in the negative sense. If there is no inspiratory fall in the central venous pressure and a fall in pulmonary artery occlusion pressure of at least 2 mm Hg, it is very unlikely that cardiac output will increase in response to fluids.

The magnitude of the “y” descent in the central venous pressure tracing provides another potential predictor of a lack of fluid responsiveness. In a small series, we found that no patient with a “y” descent of >4 mm Hg, including the “y” descent that occurs during spontaneous inspiration, had an increase in cardiac output in response to fluids (19). However, some patients with a “y” descent <4 mm Hg also did not respond to fluids; thus, once again, a prominent “y” descent indicates that the heart is operating on the plateau of its function curve and the output will not increase in response to fluids, but a value less than this does not rule out volume limitation.

Besides the assessment of volume status, the pattern of change in central venous pressure in relation to a change in cardiac output can be very useful (as long as there is no major change in pleural or abdominal pressures). If a fall in cardiac output is observed, the next question to ask is what happened to the central venous pressure, because this allows an assessment of the interaction of cardiac and return functions. If cardiac output falls with a fall in central venous pressure, the primary problem is a decrease in the return function, which most often is due to a loss of stressed vascular volume; volume infusion is likely the best therapeutic approach. If the cardiac output falls with a rise in central venous pressure, the primary problem is a decrease in pump function, and therapy should be aimed at improving pump function.

Note that in all the discussion above on fluid challenges I have referred to the central venous pressure and not the pulmonary artery occlusion pressure for the management of cardiac preload. That is because the central venous pressure indicates where the heart interacts with the returning blood. Whether cardiac limitation is due to a right-heart problem or a left-heart problem, the right atrium is the place where cardiac function interacts with the return function (6). Furthermore, the right and left hearts are in series, and once the right-heart function curve reaches a plateau, changes in left-heart function will no longer affect flow, except if the change in function alters the load on the right heart and thereby alters the plateau. The expression is “no left-sided success without right-sided success.” It is for this reason that I argue that the pulmonary artery occlusion pressure should never be used to optimize cardiac preload. Similarly, measurements of left ventricular size by echocardiography also should not be used to assess cardiac preload.

A very important distinction that must be made is the difference between cardiac output being volume-responsive and a patient's need for volume. All the discussion so far has considered how to identify volume responsiveness. The need for fluid is based on clinical parameters such as the presence of hypotension, the current use of vasopressors, and even just the need to establish volume reserves. There is a paucity of data in the literature to provide a basis for appropriate guidelines for the use of fluids for these purposes, and empirical studies are needed to provide answers.

CONCLUSIONS
The central venous pressure is there to be used by the thoughtful clinician, and as long as respect is paid to basic physiologic principles as well as principles of measurement, in my opinion it can provide a useful guide to assessment of cardiac preload, volume status, and the cause of a change in cardiac output and blood pressure.

Central Venous Pressure

Best Review (Curr Opin Crit Care 2005;11:264)

Normally CVP is negative in a normal person in upright position

Need a reference point for measurements; this is by convention the midpoint of the right atrium. Where second rib attaches tot he sternum plus 5 cm. This is true whether the patient is supine or sitting erect up to 60°

Phlebostatic point is also used, but is really only appropriate when the patient is supine.

Midaxilla point gives readings which are ~3mm Hg higher than the sternal angle

Pressure outside of the heart is the pleural pressure, not atmospheric pressure, this can obviously affect measurements

Therefore measurements should be made at end-expiration

We measure at the heart against pleural but the veins are pumping against atmospheric

Measure JVD above the sternal angle, and add 5cm of water then convert to mm Hg:

Then Divide by 1.36 (Divide by 13.6 which is the relative density of mercury and then multiply by 10 to convert cm to mm)

The CVP has three prominent positive waves: the ‘a,’ ‘c,’ and ‘v’ waves and two prominent negative waves, the ‘x’ and ‘y’ descents. The ‘a’ wave is due to atrial contraction, the ‘c’ wave is due to the backward buckling of the tricuspid valve at the onset of systole, and the ‘v’ wave is due to atrial filling during diastole. The ‘x’ descent is due to the fall in atrial pressure during relaxation of the atrial contraction. The ‘y’ descent is due to the sudden decrease in atrial pressure at the onset of diastole when the atrioventricular valve opens and allows the atrium to empty into the ventricle. The ‘y’ descent is affected by the relative filling of the atria and ventricles at the start of diastole, the compliance of the chambers, and the pressure outside the heart [18]. This last factor can be useful for marking inspiration on the hemodynamic recording in patients with spontaneous breaths, for the ‘y’ descent increases during inspiration. Prominent ‘a’ and ‘v’ waves raise the question where one should make the measurement on the tracing: at the top of the waves, the bottom, or the middle (Fig. 3). As in all pressure measurements, there is an arbitrariness of the measurement; however, the most common reason for assessing CVP is likely the assessment of cardiac preload. For this purpose, the best place for the measurement is the ‘z’ point, which is at the leading edge of the ‘c’ wave, for this gives the final pressure in the atrium and thus the ventricle just before ventricular contraction [19]. This value is often not easy to identify, however, in which case it can be closely approximated by the base of the ‘a’ wave. Timing the event from the Q wave of the electrocardiogram in turn can identify this point. It must be emphasized that this measure of CVP provides a convenient standard value that can be shared among different persons; however, there can still be important hemodynamic effects on upstream organs such as the liver and kidney from prominent ‘a’ and ‘v’ waves.

Use of the pattern of respiratory variations in central venous pressure to predict the response to a fluid challenge. Above left, tracing from a patient with an inspiratory fall in central venous pressure (CVP). Most patients with this pattern had an increase in cardiac output. Above left, tracing from a patient with no inspiratory fall in CVP. All patients but one with this pattern had no increase in cardiac output after a volume bolus. Reproduced with permission [20].

Assessment of Indices of preload and volume responsiveness (Curr Opin Crit Care 2005;11:235)

Preload does not equal preload responsiveness.

Can use antecubital cvp (Inten Care Med 2004;30:627)

Figure 2. Example of a central venous pressure (CVP) tracing with prominent “a” and “v” waves. There is a small “c” wave after the “a” wave, followed by the “x” descent. The appropriate point for measurement is the base of the “c” wave (or the “a” wave when the “c” wave cannot be seen). In this example, the difference between the bottom (the correct position) and the top is 8 mm Hg.
From:   Magder: Crit Care Med, Volume 34(8).August 2006.2224-2227

Central venous pressure is determined by the interaction of two functions: cardiac function, which represents the classic Starling length-tension relationship, and a return function, which defines the return of blood from the vascular reservoir to the heart (13). Thus the central venous pressure by itself has little meaning. The central venous pressure in a normal person in the upright posture is usually less than zero (atmospheric pressure) with a normal volume and normal cardiac function (14). However, a low central venous pressure also can indicate hypovolemia or can be present in someone who is hypervolemic (i.e., with increased return function) but has a very dynamic heart. On the other hand, a high central venous pressure can be present in someone with a high volume and normal cardiac function as well as in someone with normal volume and decreased cardiac function. Thus, a central venous pressure measurement must be interpreted in the light of a measure of cardiac output or at least a surrogate of cardiac output, such as venous oxygen saturation or pulse pressure variations. The situation is similar to the analysis of Pco2; to properly interpret the clinical meaning of Pco2, one needs to know the pH.
 

MEASURE at BASE of C WAVE or a wave if no Cs. Use end expiration.

USE OF THE CENTRAL VENOUS PRESSURE
Central venous pressure is commonly used to optimize cardiac preload. However, an essential point is that the cardiac function curve has a plateau and when that plateau is reached, further volume loading and increasing the central venous pressure will not alter cardiac output. The increase in central venous pressure will only contribute to peripheral edema and congestion of organs. The plateau is due to restriction by the pericardium, or in the absence of the pericardium, the cardiac cytoskeleton. A difficult problem for managing the care of patients is that the central venous pressure at which cardiac filling is limited is highly variable (3, 15, 16). It can occur at a central venous pressure as low as 2 mm Hg (measured relative to 5 cm below the sternal angle) but also as high as 18 to 20 mm Hg. However, as a working number, the cardiac function curve will plateau in most people by a central venous pressure of ~10 mm Hg (12–14 mm Hg when the mid-thoracic reference level is used) (9). When the central venous pressure is higher than 10 mm Hg and there is a question of the potential for a volume load to increase cardiac output, one should first consider possible reasons for why the central venous pressure is higher than normal. Explanations include chronic pulmonary hypertension, high positive end-expiratory pressure (whether external or internal), and some other restrictive processes.

The “gold standard” for determination of whether or not cardiac function is volume-limited is to perform a fluid challenge and determine whether an increase in central venous pressure results in an increase in cardiac output. For this purpose I recommend that there be an increase in central venous pressure of at least 2 mm Hg, for that magnitude of change can be recognized on most monitors. For the test to be positive there should be an increase in cardiac output of 300 mL/min, a value in the range of reproducibility of thermodilution cardiac output devices (17). In reality, even smaller changes in central venous pressure should increase cardiac output in someone whose heart is on the ascending part of the cardiac function curve. Consider someone in whom the plateau of the cardiac function curve occurs at a central venous pressure of 10 mm Hg and the cardiac output at the plateau is 5 L/min. The slope of the line connecting the plateau to the zero intercepts indicates that cardiac output should increase by 500 mL/min for every 1-mm Hg increase in central venous pressure, and that is still an underestimate of the steep part of the function curve. Furthermore, the increase in cardiac output should occur as soon as the central venous pressure is increased, for on the basis of Starling's law, an increase in end-diastolic volume will affect the stroke volume of the next beat.

If the clinical question is simply to determine whether the person is volume-responsive at a given central venous pressure, the type of fluid used for the fluid challenge is not important. What is important is to run the fluid in as fast as possible; the faster the fluid is given, the lesser has to be given. When I am concerned about giving too much volume unnecessarily, I sometimes use a pressure bag to increase the speed of the infusion, and as soon as the central venous pressure increases by 2 mm Hg, I measure the cardiac output.

An interesting approach to a volume challenge that can avoid extrinsic volume infusion is to elevate the patient's leg to provide an autotransfusion and observe the cardiac response (18). Another possible test is to perform a hepatojugular reflux (12). In this test the abdomen is compressed and the effect on jugular venous distention is observed. It has been shown that if jugular venous distention persists for more than 10 secs, it is indicative of right-heart dysfunction, and although this has not been directly studied, it would likely mean that the patient will not respond to volume.

The important clinical question with regard to fluid responsiveness in most patients should be phrased in the negative: “Is it unlikely that this patient will respond to fluids?” To this end, examination of the pattern of respiratory variations in the central venous pressure is useful to predict a lack of fluid responsiveness in patients who have spontaneous inspiratory efforts (15). This examination was also shown to be effective for patients who are mechanically ventilated but have at least some triggered efforts. The first step is to determine whether there is an adequate inspiratory effort. If the patient has a pulmonary artery catheter in place, respiratory fluctuations in pulmonary artery pressure give an indication of the adequacy of the inspiratory effort. If there is no pulmonary artery catheter, simple observation of the patient is often adequate. If the central venous pressure as measured at the base of the “a” wave falls by >1 mm Hg during inspiration and this is not due to the relaxation of expiratory muscles, usually the patient will respond to fluids, although some patients may not. However, the test is more important in the negative sense. If there is no inspiratory fall in the central venous pressure and a fall in pulmonary artery occlusion pressure of at least 2 mm Hg, it is very unlikely that cardiac output will increase in response to fluids.

The magnitude of the “y” descent in the central venous pressure tracing provides another potential predictor of a lack of fluid responsiveness. In a small series, we found that no patient with a “y” descent of >4 mm Hg, including the “y” descent that occurs during spontaneous inspiration, had an increase in cardiac output in response to fluids (19). However, some patients with a “y” descent <4 mm Hg also did not respond to fluids; thus, once again, a prominent “y” descent indicates that the heart is operating on the plateau of its function curve and the output will not increase in response to fluids, but a value less than this does not rule out volume limitation.

Besides the assessment of volume status, the pattern of change in central venous pressure in relation to a change in cardiac output can be very useful (as long as there is no major change in pleural or abdominal pressures). If a fall in cardiac output is observed, the next question to ask is what happened to the central venous pressure, because this allows an assessment of the interaction of cardiac and return functions. If cardiac output falls with a fall in central venous pressure, the primary problem is a decrease in the return function, which most often is due to a loss of stressed vascular volume; volume infusion is likely the best therapeutic approach. If the cardiac output falls with a rise in central venous pressure, the primary problem is a decrease in pump function, and therapy should be aimed at improving pump function.

Note that in all the discussion above on fluid challenges I have referred to the central venous pressure and not the pulmonary artery occlusion pressure for the management of cardiac preload. That is because the central venous pressure indicates where the heart interacts with the returning blood. Whether cardiac limitation is due to a right-heart problem or a left-heart problem, the right atrium is the place where cardiac function interacts with the return function (6). Furthermore, the right and left hearts are in series, and once the right-heart function curve reaches a plateau, changes in left-heart function will no longer affect flow, except if the change in function alters the load on the right heart and thereby alters the plateau. The expression is “no left-sided success without right-sided success.” It is for this reason that I argue that the pulmonary artery occlusion pressure should never be used to optimize cardiac preload. Similarly, measurements of left ventricular size by echocardiography also should not be used to assess cardiac preload.

A very important distinction that must be made is the difference between cardiac output being volume-responsive and a patient's need for volume. All the discussion so far has considered how to identify volume responsiveness. The need for fluid is based on clinical parameters such as the presence of hypotension, the current use of vasopressors, and even just the need to establish volume reserves. There is a paucity of data in the literature to provide a basis for appropriate guidelines for the use of fluids for these purposes, and empirical studies are needed to provide answers. (Critical Care Medicine. 34(8):2224-2227, August 2006.)

Central Venous O2 Sat (ScvO2)

Mixing of coronary sinus blood from heart is probably the reason for lower sv02 than scv02 (Chest 2004;126(6):1891)

Concordance is good (Intensive Care Med 2004;30:1572)

Importance of sampling site (Crit Care Med 1998;26(8):1356) from a study which examined patients in shock. Correlation of means was good but confidence intervals for correlation were wide.

Review Venous Oximetry (Curr Opin Crit Care 2005;11:259)

Scalea's Article (J Trauma 1990;30:1539)

River's Editorial (Chest 2006;129(3):507) value of ScvO2 is not on absolute number, but what the trend represents

Review article (Curr Opin Crit Care 2006;12:263)

really bad article saying it does not correlate with ScvO2 but then shows it does (Inten Care Med 2006;32:1336)

Pulmonary Artery Catheter Insertion

Is the PAC reallyyyy dead??

Assumptions:

CVP doesn't usually equate with with LAP

LAP does equate with PAOP if there is no mitral stenosis, no atrial regurg and a patent pulmonary vascular bed (bed distal to the catheter has to be filled with blood.

PAWP is accurate if in a Zone III area of the lung where Pa>Pv>PA(lveoli)

On X-ray, should be no more than 3-5 cm across the midline

Consider a lateral chest x-ra to make sure the cath is below the level of the left atrium (zone III)

Wedge pressure should always be less than Pulm Diastolic Pressure except in mitral regurg

when you wedge, svO2 will go up, may even match arterial.

SvO2 is not mixed venous when the balloon is up.

Catheters are not beneficial in morbidity/mortality for surgical or medical patients (NEJM 2003 Jan 2 348:5-14, JAMA 2003 Nov 26 290:2713) but they did not increase mortality either.

PAC-Man shows no clear benefit or harm to PA Caths (Lancet 2005;366:472)

If you are placing a femoral PAC in a chronic patient, get an abdominal film to assure there has been no previous placement of an IVC filter.

Escape Trial

Therapy to reduce volume overload during hospitalization for heart failure led to marked improvement in signs and symptoms of elevated filling pressures with or without the PAC. Addition of the PAC to careful clinical assessment increased anticipated adverse events, but did not affect overall mortality and hospitalization. Future trials should test noninvasive assessments with specific treatment strategies that could be used to better tailor therapy for both survival time and survival quality as valued by patients. 
(JAMA. 2005;294(13):1625-1633.)
 

The articles that started all the craze by Swan (NEJM Dec 9, 1976)

Tricuspid regurg, tamponade and right ventric fx all cause elevated RAP/CVP

tricuspid regurg should be detected by large V waves

Archives of Surgery Vol. 123 No. 8, August 1988 Archives
Pulmonary artery diastolic and wedge pressure relationships in critically ill and injured patients
R. F. Wilson, S. B. Beckman, J. G. Tyburski and D. J. Scholten
Department of Surgery, Detroit Receiving Hospital, Mich.

To study pulmonary artery wedge pressure (PAWP) and pulmonary artery diastolic pressure (PADP) relationships, we measured these simultaneously with cardiac outputs 1922 times in 128 patients who were critically ill or in an intensive care unit. In 356 (18.5%) of the readings, the PAWP exceeded the PADP, indicating that the PAWP reading might be erroneous. In 106 (5.5%) of these readings, the PAWP was 6.0 mm Hg or more higher than the PADP, indicating that the PAWP was almost certainly erroneous. In virtually all instances in which this discrepancy was recognized, changing the position of the catheter tip provided a PAWP value equal to or lower than the PADP. On the other extreme, in 49 (30%) of the patients, the PADP was 6.0 mm Hg or more higher than the PAWP. The pulmonary vascular resistance in these patients averaged (+/- SD) 257 +/- 145 dyne/s/cm-5 (normal, 80 to 160 dyne/s/cm-5). The mean pulmonary vascular resistance in the other 74 patients was significantly lower (158 +/- 72 dyne/s/cm-5). The mortality rate with the increased PADP-PAWP gradients was 59% (24/49). This was significantly higher than the mortality rate (34%, or 27/79) seen with lower PAWP-PADP gradients. Thus, the relationship between the PADP and PAWP should be examined closely in critically ill patients. A PAWP higher than the PADP indicates that the PAWP measurement may be erroneous. On the other hand, if the PADP exceeds the PAWP by 6.0 mm Hg or more, the patient has probably developed pulmonary hypertension and has a much poorer prognosis.


 

Hemodynamic Pressures

Measure all at end expiration, account for effects of PEEP

Mean Arterial Pressure

most accurate when determined by a-line

can be estimated by Diastolic BP + (pulse pressure/3)

Normal range is 85-100 mmHg

Pulse Pressure

this is what we feel when we palpate pulses

Systolic BP-Diastolic BP

increased in hyperdynamic states such as sepsis, hyperthyroid, aortic insufficiency

Central Venous Pressure

pressure of the great veins of the chest

normally between 1-7 mm Hg

equivalent to right atrial pressure

used to estimate the right ventricular preload

Right Ventricular Pressure

measured during Swann caths

Systolic is normally between 15-30 mm Hg, diastolic 1-7

Pulmonary Artery Pressure

Systolic 15-30, Diastolic 5-13, Mean 9-18

Increased values define pulmonary hypertension

Pulmonary Artery Occlusion Pressure

Normal is 4-12 mmHg

estimates the LV preload, pulmonary capillary pressure, and relative intravascular volume

Measures of Cardiac Function

Cardiac Output (CO)

volume of blood pumped by the heart into the systemic circulation each minute

Can be determined by

Thermodilution

Fick method:  CO=VO2/(10 x anDO2)

Esophageal Doppler

CO2 Rebreathing

Thoracic electrical impedance

Normally 4.5 to 6.0 L/min

Determinants

Heart Rate

Preload

Afterload

Contractility

Cardiac Index (CI)

normalizes CO to body surface area

BSA=0.007184 x Wt^0.425 x Ht^0.725

Wt in kg Ht in cm

CI=CO/BSA

Normally ranges between 2.6-4 L/min/m²

Stroke Volume (SV)

Volume of blood ejected with each heart beat

SV=100 x CO/HR

Normally 60-85 cc

Reflects the combined effects of preload, afterload, and contractility

Stroke Index (SI)

SI=SV/BSA

normally 35-50 cc/m²

Left Ventricular Stroke Work Index (LVWSI)

LVWSI=0.0136 x SI x (MSP-PAOP)

Normally 40-60 g·m/m²

a measure of the work performed by the left ventricle

Hemodynamic Resistances

Systemic Vascular Resistance (SVR)

left ventricular afterload and systemic vascular impedance

SVR=80 x (MAP-CVP)/CO

Normally 900-1400 dyne·sec/cm⁵

Systemic Vascular Resistance Index (SVRI)

SVRI=SVR x BSA

normally 1600-2400

Pulmonary Vascular Resistance (PVR)

Right Heart

CVP=Preload

PVR=Afterload

Left Heart

PAOP=Preload

SVR=Afterload

DO2=CO x CaO2(arterial blood oxygen content) x 10

Oxygen Uptake=VO2=Q x 1.34 x Hb x (SaO2-SvO2) x 10

CaO2=(1.34 cc/g x Hb g/dl x SaO2 (in 0-1)) + (0.003xPaO2)=cc/dl

Oxygen demands of the body are normally ~25% so PaO2-SvO2 should equal ~25%

SvO2 normally 65-75%

CvO2 normally 70-75%

Low Stroke Volume

Decreased Volume

Decreased Heart Contractility

Increased SVR

Decreased functioning of cardiac Valves

CO may look normal with low stroke volume and tachycardia

CVP

high CVP with low Stroke volume, think right heart failure

PAOP

RVEDV Swans

Need volumetric data

RVEF=right ventricular ejection fraction

RVEDI=right ventricular end-diastolic volume index

Independent of zero-pressure references and changing compliance

Proof cheathem et al. 2000

RVEDI=CI / (HR RVEF) or = SVI/RVEF

Incorrect placement, mitral valve disease, or irregular heart rate can still screw up the measurements

RVEDI reflects preload status

RVEF reflects contractility and afterload

PiCCO

Intens Care Med 2004;30:1377

Arterial Variation

Plethysmographic Waveform Variation

Crit Care 2005;9:R562

CCM-L Debate

PAC data is useful when it turns out that the patient needs afterload
reduction, rather than more ionotropic support, or when there is unexpected
pulmonary hypertension, and the PAOP is much lower than the CVP. In either
of these cases, the physical exam and clinical setting can be misleading. (Avi)

EVLW

The technique was revived in the 1980s and 1990s by a German company, utilizing a similar approach with a fiberoptic and thermistor-equipped 4F femoral artery catheter and thermal-dye dilution, to assess the EVLW with the help of the so-called COLD machine [6–22,23•,24•,25,26•]. The technique was later on further simplified into a single thermodilution measurement (PiCCO, Pulsion Medical Systems, Munich, FRG) [12,19,27–33,34•–36•]. The mean transit time of the thermal signal multiplied by cardiac output yields the intrathoracic thermal volume. The intrathoracic blood volume (ITBV) is derived from multiplication of the global end diastolic volume (GEDV), determined from cardiac output and down-slope time of the thermodilution curve, by a factor of 1.25, at least in humans [27]. Subtracting ITBV from intrathoracic thermal volume gives the extravascular thermal volume – EVLW (upper limit of normal about 7–10 ml/kg body weight; Table 1) [9]. The correlation in studies between ITBV and GEDV is high, even though coefficients of the regression equation relating ITBV to GEDV vary among species and, perhaps, conditions [12,27,36•,37]. The correlation is relatively high between EVLWs measured by single or double indicator dilution techniques [12,19,27].

FACTT Trial

by ARDSnet folks

Because available data are inconclusive in supporting either a fluid-liberal or a fluid-conservative approach and are also inconclusive regarding the clinical value and risks of a PAC vs a CVC in ALI/ARDS, the National Institutes of Health (NIH) ARDS Network launched the FACTT study (Fluid and Catheter Therapy Trial). The NIH ARDS Network was uniquely suited to perform such a trial. Organized in 1994 by the National Heart, Lung, and Blood Institute (NHLBI), the Network had proven successful at conducting several previous large multicenter trials examining management practices and therapies for ALI/ARDS. For FACTT, 20 academic centers were involved across North America.^[2-4]

FACTT ultimately enrolled 1000 ALI/ARDS patients and randomized them to 1 of 4 treatment strategies for 7 days. The primary end point was mortality at 60 days. Secondary end points included the number of ventilator-free days and organ-failure-free days and parameters of lung physiology. The 4 strategies were:

1. Fluid-conservative/CVC: fluids were restricted and diuretics administered to maintain a CVP < 4 mm Hg;
2. Fluid-conservative/PAC: fluids were restricted and diuretics administered to maintain a PAOP < 8 mm Hg;
3. Fluid-liberal/CVC: fluids were used to maintain a CVP between 10 and 14 mm Hg; and
4. Fluid-liberal/PAC: fluids were used to maintain a PAOP between 14 and 18 mm Hg.

In all 4 groups, explicit rules guided fluid administration, diuretics, and dobutamine usage. In addition to the CVP and PAOP targets above, other parameters that specifically guided fluid therapy were urine output (target > 0.5 mL/kg/hr), blood pressure (target of 60 mm Hg for the mean arterial pressure), and "tissue perfusion" (target cardiac index in the PAC group > 2.5 L/min/kg, targets in the CVC group included capillary refill and other physical signs). If a shock state developed (mean arterial pressure < 60 mm Hg or the need for pressors), clinicians were permitted to use whatever fluids and other therapies felt appropriate. All patients were also managed on the NIH ARDS Network low tidal volume strategy.

Results

The study concluded in late 2005. The results were released May 21, 2006, and presented at that time at the annual American Thoracic Society meeting in San Diego. They were published in The New England Journal of Medicine in the early summer of 2006. (The CVC vs PAC results were published in the May 25 issue, and the fluid-liberal vs fluid-conservative results were published in the June 15 issue.) Some of the important findings are:

One thousand patients were enrolled and randomized in the trial. The average age was 49.8 years, 53% were female, and 64% were white. The average APACHE III was 94.1, and 66% were medical ICU patients. The primary cause for lung injury was pneumonia (47%), followed by sepsis (25%) and aspiration (14%). The 4 study groups were well matched for race, comorbidities, and types of lung injury. The prerandomization fluid balance data showed that these patients were already fluid positive (mean total fluid balance was +2700 mL, mean CVP was 12.1 mm Hg, and mean PAOP was 15.6 mm Hg).

There were no differences in important outcomes in patients with PAC monitoring vs patients with CVC monitoring. However, patients with PAC monitoring had twice as many complications related to catheters compared with those with CVC monitoring (primarily nonlethal cardiac dysrhythmias). Of note, PAC was associated with significantly more blood transfusions (38% vs 30%) and a slight increase in ICU stay (0.22 days). The investigators concluded that "the use of the PAC is not indicated in the routine management of ALI/ARDS but this study does not address unusually complex patients nor the diagnostic uses of the PAC in ALI/ARDS."

Fluid Strategy

Because catheter use had no influence on results, the data from the CVC and the PAC patients in both fluid categories are combined (n = 503 in the conservative fluid group, n = 497 in the liberal fluid group) in the following discussion. Not surprisingly, the conservative fluid strategy required more than twice as much diuretic administration as the liberal fluid strategy. This resulted in a nearly even fluid balance over the 7 study days in the conservative group while the liberal fluid strategy resulted in a positive fluid balance of almost 1 L per day. Specifically, cumulative fluid balance over the first 7 days was -136 ± 491 mL in the conservative group vs 6992 ± 502 mL in the liberal group (mean ± SEM; P < .0001). Of note, this fluid-liberal result was remarkably similar to the fluid balances seen in previous NIH ARDS Network trials where fluid management was not controlled.^[2,3] This suggests that the fluid-liberal strategy likely represents "usual" clinical practice.

Mortality was not affected by fluid strategy. Specifically, 60-day mortality was 25.5% in the conservative group vs 28.4% in the liberal group (P = .3005; 95% confidence interval for the difference -2.6 to +8.4). The conservative strategy was associated with significant improvement in lung function. Specifically, this strategy improved the oxygenation index and Lung Injury Score, lowered plateau airway pressure, and increased the number of ventilator-free days (14.6 ± 0.5 vs 12.1 ± 0.5; P = .0002) and ICU-free days (13.4 ± 0.4 vs 11.2 ± 0.4; P = .0003) to day 28. These improvements were also associated with a small but significantly lower positive end-expiratory pressure requirement in the conservative fluid group.

The conservative strategy was associated with a small but significant reduction in cardiac index (primarily from a reduced stroke volume) and mean arterial pressure. This, however, did not result in a difference in mixed venous oxygenation or an increased incidence of shock. The conservative strategy was also associated with a small but significant increase in creatinine, blood urea nitrogen, and bicarbonate, but this was not associated with an increase in the incidence or prevalence of renal failure or the use of dialysis to day 60 (10% of conservative group vs 14% of liberal group; P = .0642). Indeed, the only significant difference in organ failure days was a slight reduction in central nervous system failure days in the conservative fluid group. The hemoglobin concentration was slightly increased in the conservative fluid group, but fewer patients receiving the conservative strategy were transfused (39% vs 29%).

Conclusions

The investigators concluded that "although the study did not detect a difference in mortality, the conservative fluid strategy improved lung function and shortened the duration of mechanical ventilation and intensive care stay, without increasing nonpulmonary organ failures. These results support the use of a conservative fluid management strategy in ALI/ARDS patients." In a news release from the NHLBI with the headline "For Patients With Severe Lung Injury; Less Is More," Gordon Bernard, MD, Professor of Medicine at Vanderbilt and Chair of the NIH ARDS Network Steering Committee, went on to say: "Fluid management is a complex issue, and, until now, it was not clear whether providing more or less fluids was more beneficial. Current trends in usual care appear to more closely resemble the liberal fluid management arm of this study -- the study arm with worse outcomes. This suggests that changing usual practice and adapting more conservative fluid management would better serve ALI and ARDS patients."^[4]

References

1. Connors AF, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA. 1996;276:889-897. Abstract
2. NIH ARDS Network. Ventilation with lower tidal volumes as compared to traditional tidal volumes in acute lung injury and acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308. Abstract
3. NIH ARDS Network. Higher versus lower PEEP in patients with ARDS. N Engl J Med. 2004;351:327-336. Abstract
4. NIH News Release: the FACTT Trial: May 21, 2006. Available at: http://www.nhlbi.nih.gov/new/press/06-05-22.htm. Accessed July 6, 2006.

 

 

 

sub-analysis of FACCT states physical exam not adequate for CO determination. But it actually shows that cool extremities do correlate (Crit Care Med 2009 37:2720)

picco, lidco and osophageal review (crit care 2002;6(3):216)

Heart Lung Interactions

pulsus paradoxus, increased venous from insp. causes the septum to bulge into LV decreasing SV

with mech vent, RV shrinks, but LV gets bigger with LV stroke volume increased slightly

If pulse pressure decreases with inspiration, then preload responsive to fluid, whereas if it increases with inspiration, then this reflects heart failure

(Curr Opin Crit Care 2007;13:528)

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