Introduction
Assessment of the size of the inferior vena cava (IVC) and its change in diameter in response to respiration have been investigated as a tool to screen for severe hypovolaemia [1], predict fluid responsiveness (FR) [2, 3] and assess potential intolerance to fluid loading. IVC size, collapsibility (IVCc) [2] and distensibility (IVCd) [3] have gained acceptance by emergency and intensive care unit (ICU) clinicians as FR predictors in patients with shock [4]. The ease of acquisition, reproducibility of measurements and increasing availability of ultrasound devices have supported the expansion of its use. Conflicting results have also been published [5, 6]. Injudicious application in clinical contexts where these indices have not been specifically tested may, however, mislead. On the basis of physiological principles and available, although limited, scientific evidence, it can be hypothesized that in a number of clinical conditions IVC size and/or respiratory variability may not depend on volume status and may not predict FR accurately. Although not specifically investigated yet, these conditions can be described and grouped on the basis of their main physiological determinant, as follows (Table 1) (pictorial samples are also presented as electronic supplementary material, ESM):
Ventilator settings
High PEEP and/or low tidal volumes IVCd has only been validated for the assessment of FR in mechanically ventilated patients with low levels of PEEP [3, 5]. High PEEP has been demonstrated to raise right atrial pressure (RAP), IVC pressure, and either increase or leave unaltered IVC size [7], while simultaneously reducing venous return [7], introducing a bias factor in the relationship between IVC size and FR. Furthermore, where tidal volumes less than 8 ml/kg are used, causing smaller variations in intrathoracic blood volume and pressure, IVC dimensions in response to ventilation are theoretically expected to be smaller, irrespective of volume status: available evidence suggests that IVCd shows here lower sensitivity [5] and overall inaccuracy [8] in predicting FR (Clip 1-ESM).
Patient’s inspiratory efforts
Assisted ventilation modalities/non-invasive ventilation/CPAP Inspiratory variations of IVC dimension have only been validated either in spontaneous respiration or entirely passive ventilation [2–4, 6]. These two situations share a concordant increase in abdominal pressure, and opposite (but predictable) changes in intrathoracic pressure, during inspiration. By contrast, assisted ventilation modalities/non-invasive ventilation involves a variable patient contribution to inspiration. As a result of the unpredictable interplay of ventilator-generated positive pressure and patient-generated negative pressure, IVCc loses a univocal correlation with preload [9] (Clip 2-ESM). No studies have systematically validated the IVC in determining FR in patients supported with CPAP.
Varying respiratory pattern in spontaneous breathing There are no data regarding the breathing pattern of patients with spontaneous respiration evaluated with IVCc for FR [2, 4, 6]. The amplitude of intrathoracic pressure swings and size of tidal volumes are hard to quantify in spontaneous breathing. Evidence in healthy volunteers shows that the deeper the breathing is, the larger the diaphragmatic excursions and IVCc are, irrespective of volume status [10]. This implies that shallow breaths may reduce the sensitivity of IVCc for determining FR [6], while marked inspiratory efforts seen in respiratory distress may magnify IVCc and therefore reduce its specificity (Clip 3-ESM).
Lung hyperinflation
Asthma/COPD exacerbation is associated with lung hyperinflation, development of auto-PEEP and increased intrathoracic pressure. In spontaneously breathing patients in this condition the IVC at end-expiration has been described as dilated [11]. At the same time, large negative inspiratory intrathoracic pressure swings induce IVC collapse [10]. Although not extensively investigated, these phenomena introduce a variable that affects IVC size and IVCc irrespective of central volaemia and FR. Expiratory effort (and the associated increases in abdominal pressure) may also affect IVC dimensions in an opposite manner, leading to IVC expiratory collapsibility, rather than the expected inspiratory collapse (Clip 4-ESM).
Cardiac conditions impeding venous return
Chronic RV dysfunction/tricuspid regurgitation Chronic pulmonary hypertension leads to right ventricular (RV) remodelling and decreased compliance, RAP elevation, and chronic IVC enlargement with reduced inspiratory collapse. Here, an IVC size above the validated diagnostic cut-offs for severe hypovolaemia may coexist with FR (Clip 5-ESM); data on IVC respiratory variations and FR in this population are lacking. Furthermore, patients with severe tricuspid regurgitation exhibit a dilated IVC per se, which shows no correlation with their fluid status [12].
RV myocardial infarction induces acute systolic and diastolic dysfunction and a reduction in RV compliance, partly as a result of the constrictive effect of the pericardium secondary to RV enlargement. This leads to a disproportionate increase in right side filling pressures and systemic venous congestion. In extreme conditions the right heart behaves as a passive conduit between the venous system and the left heart. The LV becomes hyperdynamic, and the patient may be volume-responsive, despite the IVC being significantly dilated [13] (Clip 6-ESM).
Cardiac tamponade Here impeded cardiac filing ensues, and there may be consequent systemic venous congestion. IVC plethora is the associated ultrasound finding (Clip 7-ESM): the finding of a fixed, dilated IVC does not equate to an absence of FR and should not preclude volume resuscitation pending definitive intervention (if required).
Increased abdominal pressure
Intra-abdominal hypertension and abdominal compartment syndrome IVC width and size variation in response to respiration are determined by its transmural pressure, under the influence of the pressure gradient between abdominal and intrathoracic compartments. Experimental evidence suggests that increased intra-abdominal pressure reduces IVC size regardless of volume status; indeed, it compresses and deforms the IVC [14], blunting the effect of mechanical inspirations on its size. Therefore, abdominal hypertension is likely to affect the reliability of IVC-based FR indices.
Other factors
Local mechanical factors: IVC restriction/compression/thrombosis/vena cava filters/ECMO cannulae Several mechanical factors have the potential to affect IVC size and its respiratory size changes, invalidating the applicability of IVC ultrasound to estimate FR. The use of VV-ECMO and VA-ECMO always entails presence of semi-rigid central venous cannula(s) occupying the IVC to a variable extent, thereby limiting its collapsibility (Clip 8-ESM). Further, negative venous pressure interferes with IVC size and respiratory dynamics, possibly to the extent of complete collapse around the cannulae. Masses compressing/occupying the vessel, vena cava filters or IVC thrombosis can equally affect physiological IVC patency and size.
Marked IVC respiratory translational motion Some patients may exhibit a pronounced lateral IVC displacement during inspiration. This can result in misalignment of the ultrasound scanning plane and thus overestimation of IVCc [15]. Where suspected, interrogation of the IVC in its short axis may assist (Clip 9-ESM).
Conclusion
Using ultrasound to evaluate the IVC as part of the haemodynamic assessment of critically ill patients appears superficially simple. However, in order to correctly guide clinical decisions it is key to understand the basis of the evidence supporting its use. Measurements must be interpreted in the context of the patient’s underlying pathophysiological status including the mode of ventilation/respiration and ventilator settings/respiratory pattern. It must always be integrated with other findings from either a systematic focused cardiac ultrasound or a comprehensive echocardiogram. Although still very useful in the patient populations where it has been validated, IVC-based assessment of FR may not be applicable to a large proportion of ICU/emergency patients. Further studies should test its accuracy in the clinical conditions described.
References
Dipti A, Soucy Z, Surana A, Chandra S (2012) Role of inferior vena cava diameter in assessment of volume status: a meta-analysis. Am J Emerg Med 30(1414–1419):e1411
Airapetian N, Maizel J, Alyamani O, Mahjoub Y, Lorne E, Levrard M, Ammenouche N, Seydi A, Tinturier F, Lobjoie E, Dupont H, Slama M (2015) Does inferior vena cava respiratory variability predict fluid responsiveness in spontaneously breathing patients? Crit Care 19:400
Barbier C, Loubieres Y, Schmit C, Hayon J, Ricome JL, Jardin F, Vieillard-Baron A (2004) Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med 30:1740–1746
Zhang Z, Xu X, Ye S, Xu L (2014) Ultrasonographic measurement of the respiratory variation in the inferior vena cava diameter is predictive of fluid responsiveness in critically ill patients: systematic review and meta-analysis. Ultrasound Med Biol 40:845–853
Charbonneau H, Riu B, Faron M, Mari A, Kurrek MM, Ruiz J, Geeraerts T, Fourcade O, Genestal M, Silva S (2014) Predicting preload responsiveness using simultaneous recordings of inferior and superior vena cavae diameters. Crit Care 18:473
Muller L, Bobbia X, Toumi M, Louart G, Molinari N, Ragonnet B, Quintard H, Leone M, Zoric L, Lefrant JY, AzuRea G (2012) Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Crit Care 16:R188
Jellinek H, Krenn H, Oczenski W, Veit F, Schwarz S, Fitzgerald RD (2000) Influence of positive airway pressure on the pressure gradient for venous return in humans. J Appl Physiol (1985) 88:926–932
Baker AK, Partridge RJ, Litton E, Ho KM (2013) Assessment of the plethysmographic variability index as a predictor of fluid responsiveness in critically ill patients: a pilot study. Anaesth Intensive Care 41:736–741
Juhl-Olsen P, Frederiksen CA, Sloth E (2012) Ultrasound assessment of inferior vena cava collapsibility is not a valid measure of preload changes during triggered positive pressure ventilation: a controlled cross-over study. Ultraschall Med 33:152–159
Gignon L, Roger C, Bastide S, Alonso S, Zieleskiewicz L, Quintard H, Zoric L, Bobbia X, Raux M, Leone M, Lefrant JY, Muller L (2016) Influence of diaphragmatic motion on inferior vena cava diameter respiratory variations in healthy volunteers. Anesthesiology. doi:10.1097/ALN.0000000000001096
Dhainaut JF, Brunet F (1987) Phasic changes of right ventricular ejection fraction in patients with acute exacerbations of chronic obstructive pulmonary disease. Intensive Care Med 13:214–215
Mandelbaum A, Ritz E (1996) Vena cava diameter measurement for estimation of dry weight in haemodialysis patients. Nephrol Dial Transpl 11(Suppl 2):24–27
Goldstein JA (2002) Pathophysiology and management of right heart ischemia. J Am Coll Cardiol 40:841–853
Cavaliere F, Cina A, Biasucci D, Costa R, Soave M, Gargaruti R, Bonomo L, Proietti R (2011) Sonographic assessment of abdominal vein dimensional and hemodynamic changes induced in human volunteers by a model of abdominal hypertension. Crit Care Med 39:344–348
Blehar DJ, Resop D, Chin B, Dayno M, Gaspari R (2012) Inferior vena cava displacement during respirophasic ultrasound imaging. Crit Ultrasound J 4:18
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Clip 1-ESM. Patient with moderate ARDS, paralyzed, ventilated in pressure control modality (PCV) with high PEEP levels. In sequence: apical 4-chamber view (A4Ch) shows a hyperdynamic left ventricle and RV systolic dysfunction (the ratio between the area of the RV and that of the LV, RVEDA/LVEDA, is 1); ventilator curves and parameters suggest a reduced respiratory system compliance (31 ml/cmH2O is the value obtained with static measurements). Ventilation is set with an I/E equal to 1:1. Small tidal volumes are consistent with a lung-protective ventilation strategy. Inferior vena cava inspiratory size change would indicate absence of fluid responsiveness (IVCd index < 18 %). However, dynamic assessment with a pulse-contour cardiac output monitoring (Vigileo™) reveals a significant increase in cardiac index following administration of a fluid bolus (500 ml crystalloids; arrow indicates beginning of the fluid challenge) (MOV 20864 kb)
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Clip 2-ESM. Inferior vena cava in a patient ventilated with pressure support ventilation (PSV). Pressure and flow ventilator curves exhibit a significant active inspiratory effort. Inferior vena cava ultrasound (IVC, subcostal long axis view) shows consistent IVC size reduction in the first phase of the inspiration, followed by a size increase in the second phase when positive pressure exerted by the ventilator prevails. A zoomed slow-motion view at the end of the clip highlights the two phases of the inspiration, with IVC size reduction (white arrow) and increase (yellow arrow). IVC-based Fluid responsiveness indices, validated in patients either in spontaneous breathing or completely passive ventilation, are in this situation clearly not applicable (MOV 16310 kb)
Clip 3-ESM. Patient with acute pulmonary oedema in respiratory distress. First spontaneously breathing and then mechanically ventilated. In sequence: subcostal inferior vena cava view (SIVC) shows a dilated IVC with great inspiratory size reduction (IVCc index 70 %), hence potentially predictive of fluid responsiveness. Subsequent SIVC view, taken immediately after an uneventful patient intubation, conversely shows similar IVC size but completely absent distensibility, suggestive of absent volume responsiveness (patient ventilated with PCV modality, PEEP = 10 cmH2O, Psupp 13 cmH2O). No fluid bolus was administered between the two scans. A passive leg raising test (PLR) assessed with pulsed-wave Doppler sampling of left ventricular outflow tract (LVOT) yielded at this a time a conclusive negative result: a negligible increase of LVOT VTI is shown (PLR: 7 % VTI increase, from 14 cm to 15 cm). Had the patient really been fluid responsive when the positive IVCc index was obtained, the shift to positive pressure ventilation would have confirmed/increased the patient’s fluid responsiveness observed in spontaneous respiration. Both IVCd index and the PLR test during mechanical ventilation conversely ruled out FR. This suggests that the wide IVC size respiratory excursions in spontaneous respiration were rather caused by the great inspiratory effort of the patient. As a side note, a small localized pericardial effusion is also visible between the right chambers and the liver (MOV 16085 kb)
Clip 4-ESM. Respiratory pattern and inferior vena cava ultrasound in a spontaneously breathing patient with acute asthma. At admission the patient presented respiratory distress associated with marked wheezing. His breathing pattern entailed deep inspirations and forced exhalations; this is manifested by pronounced contraction of abdominal muscles at expiration and is associated with a paradoxical respiratory variation of inferior vena cava (IVC) size (i.e. an expiratory collapse during spontaneous breathing). Clips and videos present simultaneous subcostal IVC views of the patient’s breathing pattern. Some hours after effective bronchodilator therapy, forced expiration had nearly disappeared. Relevant inspiratory effort was still made by the patient, and the IVC shows inspiratory collapsibility at this time (MOV 15564 kb)
Clip 5-ESM. Spontaneously breathing septic patient with chronic pulmonary hypertension, at ICU admission. In sequence: apical 4-chamber (A4Ch) and parasternal short axis views (PSAX) show a dilated and hypokinetic RV, compressing the LV; subcostal long axis view (SLAX) shows also hypertrophy of the RV free wall (yellow arrow); subcostal inferior vena cava view (SIVC) indicates small inspiratory size reduction of the IVC (negative IVCc index). Despite this, left ventricular outflow tract pulsed-wave Doppler sampling demonstrates an increase in stroke volume and cardiac output after repeated fluid challenges (total 750 ml of crystalloids) (MOV 14083 kb)
Clip 6-ESM. Patient with RV acute myocardial infarction and cardiogenic shock, mechanically ventilated in pressure control modality (PCV). In sequence: subcostal long axis view (SLAX) shows a pattern of severe RV failure: the RV is extremely dilated (the ratio between the area of the RV and that of the LV, RVEDA/LVEDA, is >1) and dramatically hypokinetic; the RV is compressing the LV and severely interferes with its filling. Subcostal inferior vena cava view (SIVC) highlights negligible respiratory distensibility of the vessel (IVCd < 18 %), i.e. a negative prediction for fluid responsiveness. On the basis of the pathophysiology of haemodynamic instability in RV myocardial infarction, 1000 ml of ringer acetate was progressively administered over 1 h. Subsequent SLAX shows an equally failing RV, but a better filled LV; SIVC view highlights persistence of a fixed, dilated IVC, which now appears even larger. Dynamic assessment with pulse-contour cardiac output monitoring (Vigileo™) confirmed a significant increase in stroke volume and cardiac index as result of the fluid bolus (arrow indicates the start of fluid bolus administration). As a side note, the hyperechoic structure floating in the RV and IVC is the wire of a temporary pacemaker (MOV 19584 kb)
Clip 7-ESM. Patient with cardiac tamponade caused by pericardial metastatic disease, spontaneously breathing. In sequence: subcostal long axis view (SLAX) shows a large circumferential pericardial effusion, a “swinging heart”, and clear signs of compression of the low-pressure heart chambers (RV wall diastolic inward displacement, RA wall systolic inward displacement). Subcostal inferior vena cava view (SIVC) confirms the diagnosis by highlighting IVC plethora, a hallmark of systemic venous congestion in tamponade. While the patient waited for a resolving emergent pericardiocentesis, a bolus of 500 ml hetastarch was administered, with a beneficial increase of non-invasive blood pressure from 70/50 mmHg to 85/55 mmHg and slight improvement in patients symptoms (MOV 13907 kb)
Clip 8-ESM. Inferior vena cava containing two ECMO cannulae in a patient supported with vv-ECMO with femoro-femoral access (patient ventilated in assisted modality, PSV). In sequence: subcostal inferior vena cava views in long axis (SIVC long) and short axis (SIVC short) cuts show the side-by-side presence of two cannulae (arrowṡ). They completely occupy the lumen of the vessel and clearly prevent the vessel’s inspiratory size reduction upon patient’s inspiration (MOV 16858 kb)
Clip 9-ESM. Patient manifesting marked inspiratory lateral translation of the inferior vena cava, generating a misleading, apparent, inspiratory collapse of the vessel (spontaneous respiration). In sequence: subcostal inferior vena cava (SIVC long) view shows a large inspiratory size reduction of the vessel. A transverse cut (SIVC short) at the same level conversely highlights an absence of respiratory variations of the IVC, unmasking the pitfall. Subsequent dynamic adjustment of the scanning plane during inspiration allows one to maintain a sagittal cut of the IVC throughout the entire respiratory cycle (SIVC long adjusted alignment). This finally leads to a correct interpretation of the ultrasound picture, depicting a negative IVC collapsibility index (MOV 23103 kb)
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Via, G., Tavazzi, G. & Price, S. Ten situations where inferior vena cava ultrasound may fail to accurately predict fluid responsiveness: a physiologically based point of view. Intensive Care Med 42, 1164–1167 (2016). https://doi.org/10.1007/s00134-016-4357-9
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DOI: https://doi.org/10.1007/s00134-016-4357-9