Vena Caval Ultrasonography. Why?

It has been well established that only about 50% of hemodynamically unstable patients are fluid responsive; i.e that they will increase their stroke volume by greater than 10% following a fluid challenge (usually 500 cc crystalloid). Consequently many static and dynamic “hemodynamic” parameters have been investigated (and adopted) as indices of fluid responsiveness. As portable ultrasound devices have become ubiquitous in the emergency department and ICU, and as these devices are “easy” to use, non-invasive and applicable to a large population of patients various ultrasonographic techniques have been studied as a marker of fluid responsiveness. As the inferior vena cava is readily visualized ultrasonographically both the vena caval diameter and its respiratory variation have been used to assess fluid responsiveness.[1]  However, based on minimal supporting evidence this technique is widely used for this purpose and likely leads to serious errors in fluid management. The validity of inferior vena caval ultrasonography in assessing fluid status will be briefly reviewed in this posting.

In healthy adult subjects, the IVC diameter averages 1.7 +/- 0.4 cm and decreases by approximately 50% during tidal breathing. Conversely, during positive pressure ventilation the diameter of the IVC increases by about 50%. The IVC diameter is determined by the difference between the internal (i.e., central venous pressure – CVP) and external pressure (intraabdominal pressure). When intraabdominal pressure is negligible, a linear positive relationship exists between the CVP and the IVC diameter. It has therefore been well established that the IVC diameter is an indirect measurement of the CVP; [5-9] that is, “the IVC is the CVP.” [2] However, it now widely accepted that the CVP is of no value for predicting volume status and fluid responsiveness.[3-5]  It would therefore appear illogical that an indirect measure of right atrial pressure (CVP) would predict fluid responsiveness; that is the IVC diameter is an indirect measure of a variable which in itself is a worthless measurement. In evaluating the maximal IVC diameter as a marker of fluid responsiveness, Airapetian et al reported an area under the receiver operating characteristic curve (ROC) of 0.62 in 58 critically ill shock patients, which is strikingly similar to that of the CVP (0.56).[6]

Due to the unreliability of the IVC diameter in predicting fluid status it was postulated that the respiratory variation in the IVC diameter (during both spontaneous and mechanical breaths) could predict fluid responsiveness. The logic of this postulate is perplexing and reflects circular and obtuse reasoning. It has been demonstrated that the degree of collapse of the IVC (during spontaneous breathing) is simply a reflection of the baseline CVP (see figures 1 and 2).[7]  The inferior vena caval distensibility index (dIVC) is calculated as the ratio of diameter of the inferior vena caval during inspiration (positive pressure) over that during expiration.[1] The use of the dIVC is based on a two small, single center study studies reported by Feissel et al (n=39) in 2003 and by Barbier et al (n=20) in 2004 who claimed that the “respiratory change in IVC diameter is an accurate predictor of fluid responsiveness.”[8,9] It should be noted that in both of these studies a tidal volume of > 8ml/kg were used. More recent studies have been unable to confirm the findings of these studies.  Ibarra-Estrada and colleagues compared a number of methods for assessing fluid responsiveness in patients undergoing mechanical ventilation with a lung protection strategy (tidal volume of 6ml/kg IBW).[10] The ROC for the dIVC and IVC diameter were 0.54 (95% CI, 0.41-0.67) and 0.52 (95% CI, 0.39-0.65) respectively which were no better than that for the CVP (0.52 (95% CI, 0.38-0.65). In the study by Airapetian quoted above, the diagnostic accuracy of the dIVC was similarly no better than that for the IVC diameter itself (ROC 0.62). [6] In the largest study to date (n=540) which evaluated the IVC collapsibility index in mechanically ventilated patients (TV of 7.8mls/kg) Vignon et al (recognized experts in the field of echocardiography) reported an AUC of 0.63, which is far below an acceptable diagnostic threshold.

The dIVC have been studied in spontaneously breathing patients and is commonly used in the emergency department in this situation. During spontaneous breathing the degree of IVC “collapse” is dependent on the CVP and the magnitude of inspiratory effort. The changes in intrathoracic pressure are much smaller than with positive pressure ventilation and likely to have a much smaller effect on the vena cava. The IVC variability has been shown to have little predictive value in patients undergoing mechanical ventilation, where the cyclical changes in intrathoracic pressure are predictable. It is therefore absurd to consider that his index would be of any value in spontaneously breathing patients with enormous variability in changes in chest volumes and pressures.  Cori et al evaluated the role of dIVC in predicting fluid responsiveness in spontaneously breathing emergency department patients.[11] In this study the dIVC was unable to predict fluid responsiveness (ROC of 0.46, 95% CI 0.21-0.71). Additional studies have demonstrated that changes in the IVC diameter and dIVC correlate poorly with changes in hemodynamics following 500 cc of blood loss in healthy volunteers.[12,13]

In conclusion, these studies suggest that the IVC diameter and dIVC should not be used to assess fluid responsiveness in both mechanically ventilated and spontaneously breathing patients. The use of these indices will result in incorrect and potentially dangerous decisions regarding fluid management. Furthermore there is no physiologic basis which could be evoked to support the use of these techniques. The diameter of the IVC and its variation with respiration are merely reflections of right atrial pressure (CVP); it is indisputable that the CVP cannot predict volume status or fluid responsiveness, so like the CVP these indices are worthless and should not be measured.  It has been argued that the IVC diameter and dIVC should not be viewed in isolation but in the context of other hemodynamic variables; this is an absurd notion as why would a clinician ever make a decision that incorporates false/misleading data.

 Addendum:

My comments should not be misconstrued that echocardiography/ultrasonography has a limited role in the ED/ICU; on the contrary, I believe it is a powerful diagnostic tool that should be available in every ICU on this planet. We published on the use of this technology in 2005 [14,15] before it had become mainstream. Bedside echocardiography performed by the emergency department physician/intensivist is critical in hemodynamically unstable patients for assessing LV and RV function and formulating a rational treatment strategy. Repeat ECHO is important in these patients to assess the impact of the intervention. Chest ultrasonography is critical in evaluating a patient with a suspected pleural effusion and in the evaluation of patients with possible pulmonary edema. Ultrasonography however has a limited role in assessing fluid responsiveness. In the hands of experts, the dynamic change in the aortic VTI is an accurate method of assessing fluid responsiveness; however, the window maybe poor in ventilated ICU patients and this methodology is very operator dependent. In those clinicians who perform vena caval ultrasonography, I would suggest moving the ultrasound probe from the abdomen to the neck.  We and other have demonstrated that changes in carotid artery Doppler flow following a fluid challenge or PLR is highly predictive of fluid responsive (see figure3).[10,16-19] In addition, the approach has been used to assess the efficiency and outcome of patients undergoing CPR. [20] This technique is easy to perform, has a very short learning curve and is highly reproducible.

In the end the most important part of the puzzle is a thoughtful clinician at the bedside who can integrate the patients’ clinical data and dynamically assess the response of the patient to therapeutic interventions. A Fool with a highly accurate diagnostic tool, is still a Fool!.

References

1. Labovitz AJ, Noble VE, Bierig M et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr 2010; 23:1225-30.
2. Kory P. Counterpoint: Should acute fluid resuscitaion be guided primarily by inferior vena cava ultrasound for patients in shock? No. Chest 2017; 151:533-36.
3. Marik PE, Baram M, Vahid B. Does the central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008; 134:172-78.
4. Marik PE, Cavallazzi R. Does the Central Venous Pressure (CVP) predict fluid responsiveness: An update meta-analysis and a plea for some common sense. Crit Care Med 2013; 41:1774-81.
5. Eskesen TG, Wetterslev M, Perner A. Systematic review including re-analyses of 1148 individual data sets of central venous pressure as a predictor of fluid responsiveness. Intensive Care Med 2015; 42:324-32.
6. Airapetian N, Maizel J, Alyamani O et al. Does inferior vena cava respiratory variability predict fluid responsiveness in spontaneously breathing patients? Crit Care 2015; 19:400.
7. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990; 66:493-96.
8. Barbier C, Loubieres Y, Schmit C et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med 2004; 30:1740-1746.
9. Feissel M, Michard F, Faller JP et al. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med 2004; 30:1834-37.
10. Ibarra-Estrada MA, Lopez-Pulgarin JA, Mijangos-Mendez JC et al. Variation in carotid peak systolic velocity predicts volume responsiveness in mechanically ventilated patients with septic shock: A prospective cohort study. Crit Ultrasound J 2015; 7:12.
11. Corl K, Napoli AM, Gardiner F. Bedside sonographic measurement of the inferior vena cava caval index is a poor predictor of fluid responsiveness in emergency department patients. Emergency Medicine Australasia 2012; 24:534-39.
12. Juhl-Olsen P, Vistisen ST, Christiansen LK et al. Ultrasound of the inferior vena cava does not predict hemodynamic response to early hemorrhage. J Emerg Med 2013; 45:592-97.
13. Resnick J, Cydulka R, Platz E et al. Ultrasound does not detect early blood loss in healthy volunteers donating blood. J Emerg Med 2011; 41:270-275.
14. Beaulieu Y, Marik PE. Bedside ultrasonography in the ICU, Part 1. Chest 2005; 128:881-95.
15. Beaulieu Y, Marik PE. Bedside ultrasonography in the ICU, Part 2. Chest 2005; 128:1766-81.
16. Marik PE, Levitov A, Young A et al. The use of NICOM (Bioreactance) and Carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients. Chest 2013; 143:364-70.
17. Ma IW, Caplin JD, Azad A et al. Correlation of carotid blood flow and corrected carotid flow time with invasive cardiac output measurements. Crit Ultrasound J 2017; 9:10.
18. Roehrig C, Gover M, Robinson J et al. Carotid artery Doppler flows correlate with cardiac output and indicate volume responsiveness following cardiac surgery. Acta Anaesthesiol Scand 2016.
19. Song Y, Kwak YL, Song JW et al. Respirophasic carotid artery peak velocity variation as a predictor of fluid responsiveness in mechanically ventilated patients with coronary artery disease. Br J Anaesth 2014; 113:61-66.
20. Adedipe AA, Fly DL, Schwitz SD et al. Carotid Doppler blood flow measurement during cardiopulmonary resuscitation is feasible: A first in man study. Resuscitation 2015.

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Paul Marik

Intensivist, Researcher, Myth-Buster, Status Quo Destabilizer

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