Clinical Review

Review: Pitfalls in Using Central Venous Pressure as a Marker of Fluid Responsiveness


 

References

Central Venous Pressure Measurement

A CVC must be placed in a sterile fashion with the tip of the catheter at the junction between the right atrium and superior vena cava. After the catheter has been properly secured and placement has been confirmed, a pressure transducer is connected from the most distal port of the CVC to the monitor. The use of CVP in the treatment of critically ill patients has logistical, mechanical, and placement issues that can complicate the clinical picture. Additionally, placement of a CVC is an invasive procedure with a set of complications that can compromise an already complex patient picture.9,10

The mechanical issues are numerous. The transducer is a water column that must be calibrated and set to zero at the level of the heart along the same plane of the right atrium (phlebostatic axis). The tip of the catheter inadvertently can be moved easily by health care workers, and a slight change in position may cause reading errors. The monitor must be recalibrated after the patient undergoes care by ancillary staff or is logrolled, moved, or repositioned in a way that affects the level of the heart. Some staff may not have adequate experience using the equipment. Misplacement of the catheter may cause erroneous and inaccurate measurements. The catheter tip must be in the right atrium, but using a catheter that is too long or short may have the catheter tip located in the superior vena cava, ventricle, or inferior vena cava (IVC). All these conditions will cause false reading of CVP.

Central Venous Pressure Interpretation

Normal CVP is 2 to 4 mm Hg, but interpretation of the value may vary. Low CVP typically indicates intravascular volume depletion and need for fluid replacement. However, caution is required with this approach. Depending on the cardiac compliance, some never have adequate volume with a low CVP and others with an elevated CVP may still augment cardiac output with additional fluid therapy (ie, a patient with hypertrophic Cardiomyopathy or advanced Pulmonary HTN).11,12

CVP as a trend may be more useful when compared to a single reading. Patients may vary on an individual basis, thereby making CVP a poor static marker. It should be used in the context of the patient’s clinical condition as it indicates the relationship between circulating blood volume and the capacity of the heart at a given time. As a trend, it is more sensitive to guide continued resuscitation efforts.13

Dynamic Techniques to Monitor Cardiac Output and Determine Fluid Responsiveness

Central venous pressure can be affected by anatomical and physiological factors such as valvular heart disease, right heart failure, poor lung compliance, or arrhythmias. In 2008, Marik et al14 performed a systematic review of 24 studies reviewing the benefits of CVP in the management of fluid therapy. In 2013, Marik et al14,15 repeated the meta-analysis of the literature which included 43 articles, and again concluded that there were no data to support the use of CVP to guide fluid therapy, and both papers conluded that CVP should not be used for fluid resuscitation. Static measures of fluid responsiveness such as CVP may not be the most appropriate measures, and may be less accurate physiologically than dynamic measures.

Dynamic measurements based on the Frank-Starling principle use the changes in the venous return (preload) and stroke volume as a marker of fluid responsiveness and may be more useful. There are several dynamic methods to assess fluid responsiveness. The first such method is the measurement of right atrial pressure. In a case series of 33 medical and surgical intensive care unit (ICU) patients who had pulmonary artery catheters, it was hypothesized that right atrial pressure predicted the response to fluid pressure as right atrial pressure should not decrease during spontaneous inspiration in patients who had a heart that was not volume responsive. Patients were classified as having a positive response test when right atrial pressure decreased ≥1 mm Hg during inspiration, or a negative response when right atrial pressure decreased <1 mm Hg. A positive response correlated with cardiac output increase of 250 mL/h.16

Evaluation of Pulse Pressure and Stroke Volume Variation

Pulse pressure variation (PPV), stroke volume variation (SVV), and variation of the amplitude of pulse oximeter plethysmographic waveform are highly predictive of fluid responsiveness in mechanically ventilated patients who have septic or hemorrhagic shock.17,18 The PPV is derived from the analysis of the arterial waveform, and SVV is derived from pulse contour analysis. The PPV uses the physiologic changes that occur during positive pressure ventilation. The delivery of a mechanical breath increases pleural pressure on inspiration, causing the following: (1) a decrease in RV preload because of decreased venous return; and (2) increase in RV afterload because of increased transpulmonary pressure. These changes lead to decreased RV stroke volume, which is at a minimal level at the end of inspiration. The inspiration reduction in RV ejection leads to a decrease in LV filling after a phase lag of two to three heart beats because of long pulmonary transit time. Thus, the LV preload reduction may induce a decrease in LV stroke volume, which is at its minimum volume during the inspiratory period of mechanical ventilation.18 The variation between the RV and LV stroke volume are greatest when the ventricles operate on the steep part of the Frank-Starling curve (rather than the flat portion). The PPV is calculated as the difference between maximum and minimum pulse pressures divided by the average of their sum, and multiplied by 100%. A variation in PPV of greater than 13% is highly predictive of volume responsiveness.19 The use of PPV is feasible in the ED because the only requirements include arterial access, measurement of the minimum and maximum pulse pressures during 30 seconds, and performance of the calculation. The PPV has been validated in different patient populations. However, the use of PPV is limited to a conventional volume control mode of ventilation and restricted to tidal volumes (TVs) over 7 mL/kg, this method of measurement was validated in patients receiving tidal volumes of at least 8 cc/kg ideal body weight—which may be higher than seen in contemporary clinical practice with more restrictive TV, ventilation strategies in patients with acute respiratory distress syndrome.20 Furthermore, patients must be ventilated passively, with heavy sedation or chemical paralysis to prevent spontaneous breathing. They must also have a normal heart rhythm. Most acute lung injury states are managed with lung protective strategy with TV of 4 to 6 mL/kg, PPV values obtained using lower TVs are less reliable and their use is not recommended.20-22

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