'Static' Measures of Intravascular Volume
The Central Venous Pressure
The central venous pressure (CVP) is frequently used to guide fluid management. Indeed, two surveys of European intensivists/anesthesiologists reported that over 90% used the CVP to guide fluid management.[17,18] A recent Canadian survey reported that 90% of intensivists use the CVP to monitor fluid resuscitation in patients with septic shock. The basis for using the CVP to guide fluid management comes from the dogma that the CVP reflects intravascular volume; specifically it is widely believed that patients with a low CVP are volume depleted while patients with a high CVP are volume overloaded. Furthermore, the '5-2' rule that was popularized in the 1970's is still widely used today for guiding fluid therapy. According to this rule, the change in CVP following a fluid challenge is used to guide subsequent fluid management decisions.
The CVP describes the pressure of blood in the thoracic vena cava near the right atrium of the heart. The CVP is a good approximation of right atrial pressure, which is a major determinant of right ventricular filling. It has therefore been assumed that the CVP is a good indicator of right ventricular preload. Furthermore, as right ventricular stroke volume determines left ventricular filling, the CVP is assumed to be an indirect measure of left ventricular preload. However, because of the changes in venous tone, intrathoracic pressures (positive end expiratory pressure, etc.), left and right ventricular compliance and geometry that occur in critically ill patients, there is a poor relationship between the CVP and right ventricular end-diastolic volume. Furthermore, the right ventricular end-diastolic volume may not reflect the patients' position on the Frank–Starling curve and therefore his/her preload reserve.
We performed a systematic review to assess the value of the CVP in directing fluid management. We identified five studies that compared the CVP with the measured circulating blood volume while 19 studies determined the relationship between the CVP/delta-CVP and the change in cardiac performance following a fluid challenge. The pooled correlation coefficient between the CVP and the measured blood volume was 0.16 (95% CI 0.03–0.28). The pooled correlation coefficient between the baseline CVP and change in stroke index/cardiac index was 0.18 (95% CI 0.08–0.28). The pooled area under the receiver operator characteristic (ROC) curve was 0.56 (95% CI 0.51–0.61). The pooled correlation between the delta-CVP and the change in stroke index/cardiac index was 0.11 (95% CI 0.015–0.21). The results of this systematic review clearly demonstrate that there is no association between the CVP and circulating blood volume, that the CVP is a poor indicator of left and right ventricular preload and that the CVP does not predict fluid responsiveness. Based on these results we believe that the CVP should no longer be routinely measured in the ICU, operating room or emergency room.
Pulmonary Artery Occlusion Pressure
Since the introduction of the pulmonary artery catheter almost 30 years ago the pulmonary artery occlusion pressure (PAOP) was assumed to be a reliable and valid indicator of left ventricular preload. However, it was not long after the introduction of the pulmonary artery catheter that studies began to appear demonstrating that the PAOP was a poor reflection of preload. Recent studies have clearly demonstrated that the PAOP is a poor predictor of preload and volume responsiveness.[16,21–23] The PAOP suffers many of the limitations of the CVP. The PAOP is a measure of left ventricular end-diastolic pressure and not LVEDV or LV preload. The use of the PAOP to measure left ventricular preload assumes a direct relationship between the left ventricular end-diastolic pressure and LVEDV. This pressure–volume curve, which describes left ventricular compliance, is normally curvilinear. Furthermore, alterations in left ventricular compliance shift the pressure–volume curve. Factors that alter left ventricular compliance include left ventricular preload, left ventricular afterload, left ventricular mass and ventricular fiber stiffness. Myocardial ischemia, sepsis, diabetes, obesity, aging, sustained tachycardia, dialysis, cardioplegia as well as other factors alter myocardial fiber stiffness. In addition, the left ventricular pressure–volume curve is affected by the degree of right ventricular filling. As the two ventricles are physically coupled by the interventricular septum and by the constraining effects of the pericardium, the end-diastolic pressure–volume curve of either ventricle is dependent upon the diastolic volume of the other. Furthermore, the PAOP is influenced by the juxtacardiac pressure, particularly if positive end expiratory pressure is used.
Left Ventricular End-diastolic Area
Transesophageal echocardiography (transgastric, mid-papillary short axis view) has been used to assess left ventricular dimensions in patients undergoing mechanical ventilation. The left ventricular end-diastolic area (LVEDA) has been shown to correlate well with the intrathoracic blood volume (ITBV) and global end-diastolic volume (GEDV),[24,25] as well as with LVEDV as measured by scintography.[26–28] An end-diastolic diameter of < 25 mm and a LVEDA of < 55 cm2 have been used to diagnose hypovolemia. While a number of studies have found the LVEDA to be a good predictor of fluid responsiveness[30–34] other studies have failed to replicate this finding.[35–40] It should be recognized that a small LVEDA does not always reflect decreased intravascular volume. Small LV volumes can be seen with restriction to filling because of decreased ventricular compliance (hypertrophy, ischemia), acute cor pulmonale [acute right ventricle (RV) dysfunction] and pericardial disease. Therefore, while the LVEDA may be an accurate measure of preload, preload does not necessarily translate into preload responsiveness. In addition to a decreased LVEDA, systolic obliteration of the LV cavity has been used as a sign of deceased preload. However, LV end-systolic cavity obliteration does not necessarily imply decreased left ventricular filling. A major limitation of echocardiography is that it provides a snapshot of ventricular function at a single period in time. Recently, a disposable transesophageal echocardiography probe that allows continuous monitoring of LV function has been developed (ClariTEE, ImaCor, Uniondale, NY, USA). Such technology allows monitoring of LV volumes and function over time, allowing the clinician to determine the response to various therapeutic interventions.
Inferior Vena Caval Diameter
The diameter of the inferior vena cava (IVC) as it enters the right atrium can be measured by subcostal echocardiography. A collapsed IVC is assumed to be indicative of volume depletion while a distended IVC is reflective of a high right atrial pressure. A number of authors have demonstrated that the mean end-diastolic IVC dimension correlates with mean right atrial pressure in both spontaneously breathing and mechanically ventilated patients.[42,43] Measurement of the IVC diameter is therefore an indirect indicator of the CVP and is associated with all the limitations of CVP measurement.
ITBV Index and GEDV Index
Transpulmonary thermodilution using a single-indicator (cold bolus) is a minimally invasive technique that allows for the computation of the cardiac output (PiCCO monitoring system, Pulsion Medical Systems, Munich, Germany). Transpulmonary thermodilution requires the use of a specific thermodilution tipped arterial catheter (usually placed in the femoral artery), which measure the change in temperature following the injection of a bolus of cold saline through a central vein (in the neck). Mathematical analysis of the transpulmonary thermodilution curve allows the calculation of the ITBV index as well as the volume of blood contained in the four chambers of the heart, called the GEDV index (GEDVI). While the GEDVI provides a good estimate of intravascular volume and preload; it has the same limitations as the LVEDA (as measured by transesophageal echocardiography) in predicting volume responsiveness.[32,38,45]
Transfusion Alter Transfusion Med. 2010;11(3):102-112. © 2010 Blackwell Publishing
Cite this: Hemodynamic Parameters to Guide Fluid Therapy - Medscape - Sep 01, 2010.