{"id":5292,"date":"2011-07-14T20:25:11","date_gmt":"2011-07-14T20:25:11","guid":{"rendered":"http:\/\/crashtext.org\/misc\/blood-pressure-cuffs.htm\/"},"modified":"2015-01-19T13:44:12","modified_gmt":"2015-01-19T18:44:12","slug":"hemodynamic-monitoring","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/resuscitation\/monitoring\/hemodynamic-monitoring.htm\/","title":{"rendered":"Hemodynamic Monitoring"},"content":{"rendered":"

for assessment of fluid responsiveness<\/a><\/p>\n

venous function and cvp<\/a><\/p>\n

Normal Hemodynamic Parameters<\/a><\/p>\n

<\/span>Blood Pressure Cuffs<\/span><\/h2>\n

How automatic blood pressure cuffs actually work (J Clin Monitoring 1991;7(1):57)<\/p>\n

During hypotension, non-invasive blood pressure cuffs were inaccurate (CCM 2013;41:34))<\/p>\n

 <\/p>\n

Chad’s and My article<\/a><\/p>\n

 <\/p>\n

CO Monitors<\/a><\/p>\n

 <\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

<\/span>Fast Flush Test<\/span><\/h2>\n

\"\"<\/a><\/p>\n

 <\/p>\n

\"\"<\/a>\"\"<\/a>\"\"<\/a>\"\"<\/a>\"\"<\/a><\/p>\n

 <\/p>\n

when patient is in profound shock, CVP increases to match mean BP<\/p>\n

 <\/p>\n

force driving fluid from periphery to heart is the elastic recoil from distended small veins and venules; this is the mean circulatory filling pressure<\/p>\n

 <\/p>\n

Normal gradient for venous return is 4-6 mmHG<\/p>\n

 <\/p>\n

Cardiac function curves plateua at <10 in normal folks<\/p>\n

 <\/p>\n

Zeroing<\/p>\n

Sets monitoring to zero relative<\/strong> to atmosphere. If ATM is 760 and CVP is 10, then it is really 770<\/p>\n

 <\/p>\n

Leveling<\/p>\n

best would be 5cm below sternal angle (angle of louis)<\/p>\n

 <\/p>\n

 <\/p>\n

Where to measure<\/p>\n

best at base of c wave<\/p>\n

use base of a wave when c is not there<\/p>\n

Use wave immediately after QRS<\/p>\n

 <\/p>\n

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)<\/p>\n

 <\/p>\n

a and v waves<\/p>\n

a wave typically larger than v wave<\/p>\n

 <\/p>\n

Great CVP article (Curr Opin Crit Care 2006;12:219)<\/p>\n

 <\/p>\n

<\/span>CVP<\/span><\/h2>\n

\"\"<\/a>\"\"<\/a><\/p>\n

 <\/p>\n

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!<\/p>\n

 <\/p>\n

Measure CVP Via the stopcock<\/strong><\/p>\n

A paradoxical consequence of the increased use of monitoring is that we ignore well-tried and reliable methods. Today, we commonly measure central venous pressure (CVP) using transducers; we forget that CVP can often be obtained from an infusion already in place. The stopcock in the infusion line is held stationary beside the head; a finger resting against the forehead can help provide the stability. With the stopcock open to atmosphere, its height is adjusted until the meniscus remains level in the open port. If respiratory fluctuation is observed and, in addition, lowering and raising the stopcock causes free flow of fluid in and out, then the height of the stopcock above the mid-axillary line represents the CVP in centimeters of water (cmH2O). Strictly, of course, the pressure is measured in centimeters of Ringer’s solution or saline, not water, but in practice this density difference is negligible.<\/p>\n

To convert cmH2O to mmHg, the height of the water column must be divided by 1.36 (or multiplied by approximately 0.75). Alternatively, to convert cmH2O to kPa, the height must be divided by 10. Precautions: If free-flow and respiratory fluctuations are not seen, the reading cannot be trusted; if the fluid flows inward freely, but not outward, then the CVP has to be lower than the final level of the meniscus; exactly how much lower cannot be assumed.<\/p>\n

 <\/p>\n

 <\/p>\n

The administration of crystalloids at different flow rates through the proximal port(s) of a multi-lumen catheter placed in the superior vena cava does not affect CVP measurement at the distal port, even in mechanically ventilated patients or patients receiving vasopressors (Intensive Care Med 2006;34(3)<\/p>\n

 <\/p>\n

Recent Art in Crit Care Med<\/h4>\n

CVP does not predict hemodynamic response in post-resus pts (Crit Care Med 2007;35(1):64)<\/p>\n

used as gold standard an increase in CCO Swan measured Card Index (< or > 15%)<\/p>\n

used 500 cc HESPAN over 20 minutes<\/p>\n

pts are already resuscitated as evidenced by changes in CVP<\/p>\n

CVP<5 was very rare<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Noninvasive Monitoring of Peripheral Perfusion<\/span><\/h3>\n

(Intens Care Med 2005;31:1316)<\/p>\n

Skin temperature<\/p>\n

NIRS<\/p>\n

 <\/p>\n

<\/span>Femoral vs. Radial Arterial Lines<\/span><\/h2>\n

Radial a-lines correlated with femoral in shock patients on vasopressors (Crit Care 2006;10:R43)<\/p>\n

But not on high-dose Norepi in this study (Shock\u00a0<\/span>Issue: Volume 40(6),\u00a0December 2013,\u00a0p 527\u2013531)<\/p>\n

 <\/p>\n

Jellinek et al. [18]<\/a>showed that if CVP is 10 mmHg or less, then cardiac output will uniformly decrease in ventilated patients in whom 10 cmH2O positive end-expiratory pressure is given. If CVP is more than 10 mmHg, however, CO may increase, remain the same or decrease<\/p>\n

(<\/p>\n

go to source: Ovid: Hadian: Curr Opin Crit Care, Volume 13(3).June 2007.318\u0096323<\/p>\n

 <\/p>\n

)<\/p>\n

 <\/p>\n

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. ——————————————————————————– 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\u00965). 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. ——————————————————————————– [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). ——————————————————————————– Another important consideration for the measurement of central venous pressure is where to make the measurement in relation to the normal \u0093a,\u0094 \u0093c,\u0094 and \u0093v\u0094 waves. The \u0093a\u0094 and \u0093v\u0094 waves can often be in the range of 8\u009610 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 \u0093c\u0094 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 \u0093c\u0094 wave cannot be identified, the base of the \u0093a\u0094 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 \u0093a\u0094 or \u0093v,\u0094 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\u009610 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. ——————————————————————————– [Help with image viewing] [Email Jumpstart To Image] Figure 2. Example of a central venous pressure (CVP) tracing with prominent \u0093a\u0094 and \u0093v\u0094 waves. There is a small \u0093c\u0094 wave after the \u0093a\u0094 wave, followed by the \u0093x\u0094 descent. The appropriate point for measurement is the base of the \u0093c\u0094 wave (or the \u0093a\u0094 wave when the \u0093c\u0094 wave cannot be seen). In this example, the difference between the bottom (the correct position) and the top is 8 mm Hg. ——————————————————————————– 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\u009614 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 \u0093gold standard\u0094 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: \u0093Is it unlikely that this patient will respond to fluids?\u0094 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 \u0093a\u0094 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 \u0093y\u0094 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 \u0093y\u0094 descent of >4 mm Hg, including the \u0093y\u0094 descent that occurs during spontaneous inspiration, had an increase in cardiac output in response to fluids (19). However, some patients with a \u0093y\u0094 descent <4 mm Hg also did not respond to fluids; thus, once again, a prominent \u0093y\u0094 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 \u0093no left-sided success without right-sided success.\u0094 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. \"\"<\/a>\"\"<\/a><\/p>\n

<\/span>Central Venous Pressure<\/span><\/h2>\n

Best Review (Curr Opin Crit Care 2005;11:264)<\/p>\n

Normally CVP is negative in a normal person in upright position<\/p>\n

\"\"<\/a>\"\"<\/a><\/p>\n

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\u00b0<\/p>\n

Phlebostatic point is also used, but is really only appropriate when the patient is supine.<\/p>\n

Midaxilla point gives readings which are ~3mm Hg higher than the sternal angle<\/p>\n

Pressure outside of the heart is the pleural pressure, not atmospheric pressure, this can obviously affect measurements<\/p>\n

Therefore measurements should be made at end-expiration<\/p>\n

We measure at the heart against pleural but the veins are pumping against atmospheric<\/p>\n

 <\/p>\n

Measure JVD above the sternal angle, and add 5cm of water then convert to mm Hg:<\/p>\n

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)<\/p>\n

 <\/p>\n

The CVP has three prominent positive waves: the \u0091a,\u0092 \u0091c,\u0092 and \u0091v\u0092 waves and two prominent negative waves, the \u0091x\u0092 and \u0091y\u0092 descents. The \u0091a\u0092 wave is due to atrial contraction, the \u0091c\u0092 wave is due to the backward buckling of the tricuspid valve at the onset of systole, and the \u0091v\u0092 wave is due to atrial filling during diastole. The \u0091x\u0092 descent is due to the fall in atrial pressure during relaxation of the atrial contraction. The \u0091y\u0092 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 \u0091y\u0092 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 \u0091y\u0092 descent increases during inspiration. Prominent \u0091a\u0092 and \u0091v\u0092 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 \u0091z\u0092 point, which is at the leading edge of the \u0091c\u0092 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 \u0091a\u0092 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 \u0091a\u0092 and \u0091v\u0092 waves.<\/p>\n

\"\"<\/a><\/p>\n

 <\/p>\n

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]. \"\"<\/a><\/p>\n

 <\/p>\n

Assessment of Indices of preload and volume responsiveness (Curr Opin Crit Care 2005;11:235)<\/p>\n

Preload does not equal preload responsiveness.<\/p>\n

Can use antecubital cvp (Inten Care Med 2004;30:627)<\/p>\n

 <\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

Figure 2. Example of a central venous pressure (CVP) tracing with prominent \u0093a\u0094 and \u0093v\u0094 waves. There is a small \u0093c\u0094 wave after the \u0093a\u0094 wave, followed by the \u0093x\u0094 descent. The appropriate point for measurement is the base of the \u0093c\u0094 wave (or the \u0093a\u0094 wave when the \u0093c\u0094 wave cannot be seen). In this example, the difference between the bottom (the correct position) and the top is 8 mm Hg. From:<\/em> \u00a0 Magder: Crit Care Med, Volume 34(8).August 2006.2224-2227<\/p>\n

 <\/p>\n

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.<\/p>\n

MEASURE at BASE of C WAVE or a wave if no Cs. Use end expiration.<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

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\u009614 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 \u0093gold standard\u0094 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.<\/strong> The important clinical question with regard to fluid responsiveness in most patients should be phrased in the negative: \u0093Is it unlikely that this patient will respond to fluids?\u0094 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 \u0093a\u0094 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 \u0093y\u0094 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 \u0093y\u0094 descent of >4 mm Hg, including the \u0093y\u0094 descent that occurs during spontaneous inspiration, had an increase in cardiac output in response to fluids (19). However, some patients with a \u0093y\u0094 descent <4 mm Hg also did not respond to fluids; thus, once again, a prominent \u0093y\u0094 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 \u0093no left-sided success without right-sided success.\u0094 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.)<\/p>\n

 <\/p>\n

 <\/p>\n

most of the CVP as horrible marker literature may be due to people using the crappy machine interpretation rather than real cvp measurements (Shock 2010;33(3):253)<\/p>\n

<\/span>Central Venous O2 Sat (ScvO2)<\/span><\/h2>\n

Absolute best review of ScvO2 and Svo2<\/a><\/p>\n

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

Concordance is good (Intensive Care Med 2004;30:1572)<\/p>\n

 <\/p>\n

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.<\/p>\n

 <\/p>\n

Femoral doesn’t correlate for central (CCM 2012;40:3196)<\/p>\n

 <\/p>\n

Review Venous Oximetry (Curr Opin Crit Care 2005;11:259)<\/p>\n

 <\/p>\n

Scalea’s Article (J Trauma 1990;30:1539)<\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

 <\/p>\n

River’s Editorial (Chest 2006;129(3):507) value of ScvO2 is not on absolute number, but what the trend represents<\/p>\n

<\/span> Respiration. \u00a02001; 68(3):279-85<\/strong>\u00a0(ISSN: 0025-7931)<\/span><\/h3>\n

Ladakis\u00a0C; Myrianthefs\u00a0P; Karabinis\u00a0A; Karatzas\u00a0G; Dosios\u00a0T; Fildissis\u00a0G; Gogas\u00a0J; Baltopoulos\u00a0G Athens University School of Nursing Intensive Care Unit at Agioi Anargyroi Cancer Hospital of Kifissia, Athens, Greece.<\/p>\n

BACKGROUND: Although mixed venous O2 saturation (SvO2) accurately indicates the balance of O2 supply\/demand and provides an index of tissue oxygenation, the use of a pulmonary artery (PA) catheter is associated with significant costs, risks and complications. Central venous O2 saturation (ScvO2), obtained in a less risky and costly manner, can be an attractive alternative to SvO2. OBJECTIVES: To investigate whether the values of ScvO2 and SvO2 are well correlated and interchangeable in the evaluation of critically ill ICU patients and to create an equation that could estimate SvO2 from ScvO2. METHODS: Sixty-one mechanically ventilated patients were catheterized upon admission and ScvO2 and SvO2 values were simultaneously measured in the lower part of the superior vena cava and PA respectively. RESULTS: SvO2 was 68.6 +\/- 1.2% (mean +\/- SEM) and ScvO2 was 69.4 +\/- 1.1%. The difference is statistically significant (p < 0.03). The correlation coefficient r is 0.945 for the total population, 0.937 and 0.950 in surgical and medical patients, respectively. In 90.2% of patients the difference was <5%. When regression analysis was performed, among 11 models tested, power model [SvO2 = b0(ScvO2)b1] best described the relationship between the two parameters (R2 = 0.917). CONCLUSIONS: ScvO2 and SvO2 are closely related and are interchangeable for the initial evaluation of critically ill patients even if cardiac indices are different. SvO2 can be estimated with great accuracy by ScvO2 in 92% of the patients using a power model.<\/p>\n

 <\/p>\n

Review article (Curr Opin Crit Care 2006;12:263)<\/p>\n

 <\/p>\n

 <\/p>\n

really bad article saying it does not correlate with ScvO2 but then shows it does (Inten Care Med 2006;32:1336)<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Hemodynamic Pressures<\/span><\/h2>\n

Measure all at end expiration, account for effects of PEEP<\/p>\n

<\/span>Mean Arterial Pressure<\/span><\/h3>\n

most accurate when determined by a-line<\/p>\n

can be estimated by Diastolic BP + (pulse pressure\/3)<\/p>\n

Normal range is 85-100 mmHg<\/p>\n

<\/span>Pulse Pressure<\/span><\/h3>\n

this is what we feel when we palpate pulses<\/p>\n

Systolic BP-Diastolic BP<\/p>\n

increased in hyperdynamic states such as sepsis, hyperthyroid, aortic insufficiency<\/p>\n

<\/span>Central Venous Pressure<\/span><\/h3>\n

pressure of the great veins of the chest<\/p>\n

normally between 1-7 mm Hg<\/strong><\/p>\n

equivalent to right atrial pressure<\/p>\n

used to estimate the right ventricular preload<\/p>\n

<\/span>Right Ventricular Pressure<\/span><\/h3>\n

measured during Swann caths<\/p>\n

Systolic is normally between 15-30 mm Hg, diastolic 1-7<\/p>\n

<\/span>Pulmonary Artery Pressure<\/span><\/h3>\n

Systolic 15-30, Diastolic 5-13, Mean 9-18<\/p>\n

Increased values define pulmonary hypertension<\/p>\n

<\/span>Pulmonary Artery Occlusion Pressure<\/span><\/h3>\n

Normal is 4-12 mmHg<\/strong><\/p>\n

estimates the LV preload, pulmonary capillary pressure, and relative intravascular volume<\/p>\n

 <\/p>\n

<\/span>Measures of Cardiac Function<\/span><\/h2>\n

<\/span>Cardiac Output (CO)<\/span><\/h3>\n

volume of blood pumped by the heart into the systemic circulation each minute<\/p>\n

Can be determined by<\/p>\n

Thermodilution<\/p>\n

Fick method:\u00a0 CO=VO2\/(10 x anDO2)<\/p>\n

Esophageal Doppler<\/p>\n

CO2 Rebreathing<\/p>\n

Thoracic electrical impedance<\/p>\n

Normally 4.5 to 6.0 L\/min<\/strong><\/p>\n

Determinants<\/h4>\n

Heart Rate<\/p>\n

Preload<\/p>\n

Afterload<\/p>\n

Contractility<\/p>\n

<\/span>Cardiac Index (CI)<\/span><\/h3>\n

normalizes CO to body surface area<\/p>\n

BSA=0.007184 x Wt0.425 x Ht0.725<\/p>\n

Wt in kg Ht in cm<\/p>\n

CI=CO\/BSA<\/p>\n

Normally ranges between 2.6-4 L\/min\/m2<\/strong><\/p>\n

<\/span>Stroke Volume (SV)<\/span><\/h3>\n

Volume of blood ejected with each heart beat<\/p>\n

SV=100 x CO\/HR<\/p>\n

Normally 60-85 cc<\/strong><\/p>\n

Reflects the combined effects of preload, afterload, and contractility<\/p>\n

<\/span>Stroke Index (SI)<\/span><\/h3>\n

SI=SV\/BSA<\/p>\n

normally 35-50 cc\/m2<\/strong><\/p>\n

<\/span>Left Ventricular Stroke Work Index (LVWSI)<\/span><\/h3>\n

LVWSI=0.0136 x SI x (MSP-PAOP)<\/p>\n

Normally 40-60 g\u00b7m\/m2<\/strong><\/p>\n

a measure of the work performed by the left ventricle<\/p>\n

<\/span>Hemodynamic Resistances<\/span><\/h2>\n

<\/span>Systemic Vascular Resistance (SVR)<\/span><\/h3>\n

left ventricular afterload and systemic vascular impedance<\/p>\n

SVR=80 x (MAP-CVP)\/CO<\/p>\n

Normally 900-1400 dyne\u00b7sec\/cm5<\/strong><\/p>\n

<\/span>Systemic Vascular Resistance Index (SVRI)<\/span><\/h3>\n

SVRI=SVR x BSA<\/p>\n

normally 1600-2400<\/p>\n

 <\/p>\n

<\/span>Pulmonary Vascular Resistance (PVR)<\/span><\/h3>\n

 <\/p>\n

Right Heart<\/p>\n

CVP=Preload<\/p>\n

PVR=Afterload<\/p>\n

 <\/p>\n

Left Heart<\/p>\n

PAOP=Preload<\/p>\n

SVR=Afterload<\/p>\n

 <\/p>\n

DO2=CO x CaO2(arterial blood oxygen content) x 10<\/p>\n

 <\/p>\n

Oxygen Uptake=VO2=Q x 1.34 x Hb x (SaO2-SvO2) x 10<\/p>\n

 <\/p>\n

CaO2=(1.34 cc\/g x Hb g\/dl x SaO2 (in 0-1)) + (0.003xPaO2)=cc\/dl<\/p>\n

 <\/p>\n

Oxygen demands of the body are normally ~25% so PaO2-SvO2 should equal ~25%<\/p>\n

 <\/p>\n

SvO2 normally 65-75%<\/strong><\/p>\n

ScvO2 normally 70-75%<\/strong><\/p>\n

 <\/p>\n

SvO2 60-75 SV 50-100 SI 25-45 CO 4-8 CI 2.5-5.0 CVP 2-6 PAP 25\/10 PAOP 8-12 SVR 900-1300 PVR 40-150 MAP 70-110<\/p>\n

 <\/p>\n

Low Stroke Volume<\/p>\n

Decreased Volume<\/p>\n

Decreased Heart Contractility<\/p>\n

Increased SVR<\/p>\n

Decreased functioning of cardiac Valves<\/p>\n

 <\/p>\n

CO may look normal with low stroke volume and tachycardia<\/p>\n

 <\/p>\n

CVP<\/p>\n

high CVP with low Stroke volume, think right heart failure<\/p>\n

 <\/p>\n

PAOP<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>PiCCO<\/span><\/h2>\n

Intens Care Med 2004;30:1377<\/p>\n

\"\"<\/a>\"\"<\/a><\/p>\n

 <\/p>\n

Arterial Variation<\/p>\n

 <\/p>\n

Plethysmographic Waveform Variation<\/p>\n

Crit Care 2005;9:R562<\/p>\n

 <\/p>\n

CCM-L Debate<\/p>\n

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)<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>EVLW<\/span><\/h2>\n

The bedside method to directly assess the amount of extravascular lung water (EVLW) as a measure of pulmonary edema in critically ill patients, which has been applied most often, is the assessment of extravascular thermal volume with the help of transpulmonary thermal-dye indicator dilution, formerly involving a dye and a cold solution, central venous bolus infection and detection in the aorta via a femoral artery catheter of the respective dilution curves [2]<\/a>. The differences in dilution curves between the intravascular dye and the cold, of which some dissipates into the pulmonary structures, dependent on their hydration status, and thus the difference in mean transit times multiplied by cardiac output, yield an extravascular thermal distribution volume as a rough indicator of EVLW \u0096 pulmonary edema. Using the Edwards densitometer technique, Mihm et al. [5]<\/a> and others already noted that the EVLW overestimated gravimetric EVLW at a postmortem examination \u0096 the gold standard in dogs and human organ donors, regardless of the cause of edema, that is hydrostatic forces or increased permeability. Nevertheless, the correlation, over a wide range of volumes, between the two was high [5]<\/a>.<\/p>\n

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\u009622,23\u0095,24\u0095,25,26\u0095]<\/a>. The technique was later on further simplified into a single thermodilution measurement (PiCCO, Pulsion Medical Systems, Munich, FRG) [12,19,27\u009633,34\u0095\u009636\u0095]<\/a>. 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]<\/a>. Subtracting ITBV from intrathoracic thermal volume gives the extravascular thermal volume \u0096 EVLW (upper limit of normal about 7\u009610 ml\/kg body weight; Table 1<\/a>) [9]<\/a>. 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\u0095,37]<\/a>. The correlation is relatively high between EVLWs measured by single or double indicator dilution techniques [12,19,27]<\/a>.<\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

picco, lidco and osophageal review (crit care 2002;6(3):216)<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Heart Lung Interactions<\/span><\/h2>\n

pulsus paradoxus, increased venous from insp. causes the septum to bulge into LV decreasing SV<\/p>\n

with mech vent, RV shrinks, but LV gets bigger with LV stroke volume increased slightly<\/p>\n

 <\/p>\n

If pulse pressure decreases with inspiration, then preload responsive to fluid, whereas if it increases with inspiration, then this reflects heart failure<\/p>\n

(Curr Opin Crit Care 2007;13:528)<\/p>\n

 <\/p>\n

 <\/p>\n

<\/span>Flo Trac<\/span><\/h2>\n

not accurate in patients with altered SVR (www.ncbi.nlm.nih.gov\/pubmed\/23479677)<\/p>\n","protected":false},"excerpt":{"rendered":"

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