Volume status and preload responsiveness assessment
A reliable assessment of volume status in the haemodynamically unstable patient is valuable in guiding management. Many a times, a more crucial question to answer is whether, the patient will respond to a bolus of fluids by raising his cardiac output, blood pressure or both. The echocardiogram can be used to answer both these questions.
The following measurements and indices are used for this purpose:
2.IVC collapsibility index
3.LV end diastolic area
4.LVOT VTI variation with respiration
5.Peripheral artery Vmax variation
6.LVOT VTI variation with passive leg raise
IVC diameter and variability
Echocardiography of the IVC can easily be done by a transthoracic, subcostal approach. The transducer position is just below the xiphisternum 1-2cms to the right of the midline, with the marker dot pointing towards the sternal notch.
Recorded using two-dimensional and M-mode echocardiography. The transthoracic probe sensor must be positioned subcostally and slowly turned 90° counter clockwise till the optimal view is obtained.
After obtaining a 2-D image of the IVC entering the right atrium and verifying that the IVC visualization is not lost during movements of respiration, place a M-mode line through the IVC 1 cm caudal from its junction with the hepatic vein, and obtain a M-mode tracing. This placement ensures that we do not measure the intrathoracic ICV dring any part of the respiratory cycle.
If the patient is spontaneously breathing, ask him to take a short quick inspiratory effort ("a sniff") during the M-mode recording. If the patient is mechanically ventilated, record the M-mode through 3 or 4 respiratory cycles.
Freeze the M-mode image and using calipers, measure the maximum and minimum diameter of the IVC tracing.
Low CVP is increasingly is likely as IVC diameter (IVCD) gets smaller than 1 cm and abnormally high CVP increasingly likely as IVCD increases above 2cm. However, there is wide variation and the absolute measurements are not applicable with positive pressure ventilation. The IVC size is an indicator of volume status and not volume responsiveness - these two are not the same.
Sometimes the IVC is completely collapsed and may be difficult to visualize (virtual IVC). Such a situation in a mechanically ventilated or spontaneously breathing patient always indicates severe hypovolemia in the absence of raised intra-abdominal pressure.
IVC collapsibility index
Measurement of IVC diameter in different phases of respiration differentiates normal subjects from patients with elevated right atrial pressure. In a spontaneously breathing, healthy subject, cyclic variations in pleural pressure, which are transmitted to the right atrium, produce cyclic variations in venous return, which is increased by inspiration, leading to an inspiratory reduction of about 50% in IVC diameter.
IVC diameter decreases on each inspiration.
The relation pressure/IVC diameter is characterized by an initial ascending curve (arrow 1) where the compliance index (slope) does not vary, and an almost horizontal end part where the compliance index progressively decreases, because of the distension.
When the IVC is dilated, the relation between the diameter and pressure is located on the horizontal part of the curve: respiratory variations in diameter, produced by a low inspiratory pressure, are therefore abolished. This is what is seen in cardiac tamponade, and in severe right ventricular failure.
The IVC collapsibility index is expressed as the difference between the value of the maximum diameter and the minimum diameter, divided by the maximum of the two values. It should be noted that the denominator here is the maximum diameter. This index is used only for spontaneously breathing non ventilated patients. This is an index of volume status (hypovolemia, hypervolemia) and right atrial pressure, but has never been studied as an indicator of volume responsiveness. Its most studied uses include estimating CVP non-invasively and monitoring fluid removal during hemodialysis and ultrafiltration.
Mechanically ventilated patients:
In a patient requiring ventilatory support, the inspiratory phase induces an increase in pleural pressure, which is transmitted to the right atrium, thus reducing venous return. The result is an inversion of the cyclic changes in IVC diameter, leading to increases in the inspiratory phase and decreases in the expiratory phase. The respiratory variations in IVC diameter in a mechanically ventilated patient are therefore only observed when right atrial pressure is normal, that is low. In a patient presenting with signs of circulatory insufficiency, this finding may indicate hypovolemia. Measurement of IVC diameter in a patient receiving mechanical ventilation does not accurately predict right atrial pressure. Absence of respiratory variations in IVC diameter in a mechanically ventilated patient presenting with signs of circulatory insufficiency suggests that volume expansion will be ineffective in 90% of cases.This variation is quantified by measuring the difference between the maximum and minimum diameters on the M-mode tracing and dividing it by the mean of the two. This is referred to as ΔIVC. It should be noted that the denominator here is the mean diameter.
In mechanically ventilated patients, a 12% or more variation identified patients likely to respond to vascular filling, in terms of increased cardiac output, from those who would not respond, with a positive predictive value of 93% and a negative predictive value of 92%. It must be remembered that the measurements should be taken during mandatory ventilator breaths and the tidal volume should be at least 8 ml/kgwith the patient in sinus rhythm.
Some others use another index called the distensibility index. This differs from ΔIVC in that the denominator is the minimum diameter. The cutoff for this index is 18%.
In spontaneously breathing patients, the normal IVC variation is approximately 50%. These two indices are not reliable in spontaneously breathing patients. Other markers of volume responsiveness in such patients are discussed below.
The great merit of this technique is that it is a dynamic, noninvasive parameter to evaluate the potential benefit of volume expansion. Moreover, the examination of the IVC is particularly easy and can be done by someone with limited experience in echocardiography.
Left Ventricular end diastolic area (LVEDA)
First, obtain a 2-D parasternal short axis view at the level of the papillary muscles. Freeze it and scroll back and forth to identify a frame showing the left ventricle in end diastole. You can use the ECG to time this. Using a caliper, trace along the endocardium to measure the area of the left ventricle at end diastole. You do not have to trace around the papillary muscles and they can be included inside the circle.
An LVEDA of less than 10cm2 or a LVEDA index (LVEDA / BSA) of less than 5.5cm2/m2 indicates significant hypovolaemia.
Another sign that suggests severe hypovolaemia is the "kissing papillar muscle sign" where opposing papillary muscles come in contact with each other at end systole.
One thing to remember is that severe concentric hypertrophy can reduce LVEDA even without any hypovolaemia.
An LVEDA of more than 20cm2 suggests a volume overload.
Left ventricular outflow tract (LVOT) Velocity Time Integral (VTI) variation with respiration
In the apical 5-chamber view, place a PWD sample volume in the middle of the LVOT just adjacent to the aortic valve. The sample cursor should not overlie the valve. Obtain a PWD tracing. Make sure there is no valve opening artifact in front of the systolic flow waveform. That means that the cursor is placed over the aortic valve and needs to be moved into the LVOT by a few millimeters.
Once you have obtained the waveform over 3 or 4 respiratory cycles, freeze the image. Reducing the horizontal sweep speed enables capture of a larger number of LVOT ejections. Scroll back and forth till you can identify the largest (usually at end inspiration, if mechanically ventilated) and the smallest waveforms over a single respiratory cycle. Go to ‘calculations'...'aortic continuity equation'....'LVOT VTI' and trace the edge of the waveforms using the trackball.
The machine will calculate the VTIs for these two waveforms. The VTI variation is then calculated as the difference between the maximum and the minimum VTI divided by the mean of the two values.
A VTI variation of more than 12% predicts fluid responsiveness (defined as an increase in cardiac output by at least 15% in response to a standard fluid bolus) with a sensitivity of 100% and a specificity of 89%.
An alternative to tracing the VTIs is to measure the maximum and minimum peak velocities (Vmax) instead. This is quicker and easier, and again, more than 12% variation suggests fluid responsiveness.
Peripheral artery Vmax variation
Some have validated respiratory variation of peak velocities (Vmax) measured with a Doppler probe in peripheral arteries such as the brachial artery, the cutoff being 10%, with a sensitivity of 74% and a specificity of 95%. This is a quick and simple way of assessing fluid responsiveness.
Left ventricular outflow tract (LVOT) Velocity Time Integral (VTI) increase with Passive Leg Raise (PLR)
The LVOT VTI is measured with a PWD in the A5C view as described above with the patient in semi-recumbent position (head up 45°). 2 assistants then lift both lower limbs of the patient to a 45° angle. A repeat LVOT VTI is measured after 1 minute.
Passive leg elevation (PLR to 45°) induced increase in VTI by > 12.5% predicts an increase in stroke volume by > 15% after saline infusion (500ml over 15minutes). The sensitivity of PLR induced response is 77% and the specificity is 100%.
Other sonological indices which can be measured during a PLR include LVOT Vmax, Femoral Vmax and aortic Vmax.