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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- Beaulieu Y, Marik PE. Bedside ultrasonography in the ICU, Part 1. Chest 2005; 128:881-95.
- Beaulieu Y, Marik PE. Bedside ultrasonography in the ICU, Part 2. Chest 2005; 128:1766-81.
- 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.
- 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.
- 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.
- 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.
- 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.
Paul Marik
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Hi. Any thoughts on measuring the ivc with the patient sitting up at 45 degress and then lying the patient down with legs up and then seeing if the ivc distensds on ultrasound.
The diameter of the IVC and is variation with respiration are indirect indicators of the right atrial pressure (CVP). It is indisputable that the CVP has no value in assessing volume status or fluid responsiveness so it is illogical to postulate that these IVC indices should be of greater diagnostic value that the CVP itself. It has been clearly demonstrated that changes in the CVP following an intervention (fluid bolus, PLR, etc) do not improve the diagnostic ability of the CVP; it would be reasonable to assume that chances in diameter of the IVC after similar interventions would not be useful.
This is a good review and will make me go back and look at some of the Romany literature and reviews on other sites.
Even though it gets talked about a lot I doubt IVC ultrasound is actually used as ubiquitously as you might think in EDs for all or even the majority of patients with sepsis.
I agree that doing things for sepsis patients “based on minimal supporting evidence” is not good.
Primary not Romany
John. Thanks for your comments. From the Twitter storm that this post has ignited, I suspect many clinicians (who are attempting to justify the use of IVC ultrasonography) do actually use this technique in clinical practice. I would be interested if you can find any primary literature that can support this practice.
Thanks for a Useful post. How are you assessing fluid responsiveness at the bedside in septic patients. When using plr are you using LVOTVTI or etco2 or MAP to show a positive response? Is this valid in spont breathing pts, non paralysed pts, non intubated patients etc?
Tom: Good question (and see my updated post). We use a number of methods to assess fluid responsiveness including change in MAP AND the change in SV using the NICOM or PiCCO monitors. We have also used the change in carotid flow velocity (see updated post). For those with expertise in echocardiography the change in aortic VTI is an accurate indicator of fluid responsiveness. Changes in end-tidal CO2 have been shown to be predictive of fluid responsiveness, however, the changes are quite small and may be difficult to detect; furthermore, this method may be less reliable in patients with a large intra-pulmonary shunt. While the ultimate goal of a fluid challenge is to increase the MAP (in patients with a MAP less 65mmHg) it is important to recognize that in patients with sepsis a fluid challenge may result in further vasodilatation; i.e the SV may go up, but the SVRI goes down and the MAP stays the same; therefore the change in MAP may not be a good indicator of the change in SV..
Dr. Marik, can you kindly reference your statement that a fluid bolus “may result in further vasodilation?” Since cardiac output is inversely related to SVR, SVR is inversely related to blood viscosity, and MAP is essentially the product of cardiac output and SVR added to the CVP, I would be interested as to how vasodilation is implicated as the cause of a decrease in SVR rather than the decrease in blood viscosity that accompanies a crystalloid infusion (as both may result in a similar increase in CO and decrease in SVR with a stable MAP). I appreciate that all this is pointless if the intervention only results in interstitial edema anyway, but I took your comment as intriguing from a physiology point of view.
Monge-Garcia et al measured the effects of a fluid bolus on arterial load in patients with septic shock.[1] In this study 67% of patients were fluid responders, however the MAP increased in only 44% of these patients (pressure responder). Overall there was a significant fall in effective arterial elastance (Ea) and systemic vascular resistance (SVR), this effect being most marked in the pre-load responders who were pressure non-responders. Additional studies have demonstrated a fall in SVR following fluid resuscitation in patients with sepsis.[2,3] This suggests that fluid boluses should be considered vasodilator therapy in patients with sepsis and that aggressive fluid resuscitation may potentiate the hyperdynamic state.
References
1. Monge-Garcia MI, Gonzalez PG, Romero MG et al. Effects of fluid administration on arterial load in septic shock patients. Intensive Care Med 2015; 41:1247-55.
2. Pierrakos C, Velissaris D, Scolletta S et al. Can changes in arterial pressure be used to detect changes in cardiac index during fluid challenge in patients with septic shock? Intensive Care Med 2012; 38:422-28.
3. Monnet X, Chemla D, Osman D et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med 2007; 35:477-82.
Perfect, thank you so much!
Totally agree with the dangers of trying to use a surrogate of CVP to predict fluid response. BUT, as with CVP, to understand it as a SECURITY LIMIT, to know when to stop the use of fluids (or not to give them) could be a valid interpretation. Critical pt with high CVP do worse (R atrial pr opposed to mean systemic pr). To know that the heart of the pt with distended and non collapsing VC can’t tolerate fluids (high cvp) could still be useful in practice. It’s just another factor to consider (with capillary filling, PLR, heart echo, skin temperature, lactate, etc etc etc). It is useful when the physio is understood.
I agree with this. I think throwing the IVC collapsibility out isn’t completely warranted. Its part of the whole puzzle as to the hemodynamic status of a patient. I think that looking at the IVC and then rotating the probe to look at the RV and LV can give a good idea even to a relatively novice at ultrasound as to whether the patient can particularly tolerate fluid. I don’t think that it particularly susses out who will respond though. I think we should be teaching students and residents that if you are resuscitating a patient, make sure that crystalloid first is safe, and if they remain hypotensive after an initial bolus just start your pressor and don’t leave them hypotensive.
Getting at which patients are actually going to increase their cardiac output and be a fluid “responder” is a much more difficult question to answer.
With the knowledge that the CVP is unreliable to answer the question whether fluids is useful for a sepsis case, coupled with the knowledge that hypotension in sepsis is vasodilatory, we seem to be heading towards the question: “Should giving fluids in hypotensive sepsis cases be still routinely practiced?”. If the answer is yes, then it will be a challenge for the general physician who is without bedside echocardiogram machine, except from a phone call away from an intensivist.
Roland. You are exactly correct; this decision is a conundrum and should not be made lightly and should not result in the reflex of giving a 30ml/kg fluid bolus. . However, what I would suggest in circumstances where the clinician has limited technology is to go back to basics. If the patient is hypotensive (MAP < 65 mmHg) and not in respiratory distress, I would give a 500cc bolus of LR and closely monitor the response. If no improvement I would start norepinephrine (early via a peripheral line). If the patient does appear to respond to the fluid bolus I would cautiously repeat; once again closely monitoring the response. In the acute setting I would not give more than 3 X 500cc boluses until one can obtain additional hemodynamic data. Preliminary data suggests that the early use of norepinephrine in vasodilatory shock (not cold shock) improves outcome; our data tends to support this concept.
Dr. Marik, you’ve hit the nail on the head. Dogma dies hard; keep up the good work
I work in a hospital where CVP is followed almost religiously as method of measuring fluid responsiveness (which drives me crazy) I believe it’s quite common knowledge that it is not a reliable method for this purpose. However, I am wondering if there is any merit to using CVP as a stopping point or “non-starter” point for fluid administration? (Come across this almost daily as well) i.e. Patient has clinical signs of hypovolemia: low BP, tachycardia, cold periphery, diminishing diuresis … but “normal” CVP therefore fluids are restricted or stopped.
Ale: Good question. Should one ever measure the CVP (a bizarre thing to do); one should use it as a stopping rule for fluid administration. There is overwhelming and reproducible data that a CVP > 8 mmHg (the target for EGDT and SSC) is associated with an increased risk of acute kidney failure (AKI), progression of AKI and death. So if you measure the CVP, stop giving fluid when the CVP exceeds 8mmHg. Michael Pinsky et al have written a paper endorsing this concept. .
Pinsky MR, Kellum JA, Bellomo R. Central venous pressure is a stopping rule, not a target of fluid resuscitation. Crit Care Resus 2014; 16:245-46.
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Excellent article sir.. As usual another bold n beautiful review.. Another myth busting statement.. Looking at all the negative trials ( and LESS IS MORE trials) tht are coming up looks like we will be left with nothing/ no more gadgets n just follow the bed side measures to save the pt…
Thanks for your comments. I have written a post Entitled “Less is More”… which i will post in a few days…. I am waiting for the storm to settle after my last post. I agree, we need to get back to basics, Take a Good History and Examine the patient… seems like patients go through the “diagnsotic doughnut” before an H&P is ever done.
[…] iSepsis – Vena Caval Ultrasonography – Just Don’t Do It! […]
I’m told it’s okay to EAT the vena cava, is this true?
I am sure that it would not “taste” too good. However, I would defer this question to Scott as he may have more expertise in this area.
[…] [Blog] Marik PE. Vena Caval Ultrasound- Just don’t do it! […]
[…] I was delighted to read Dr. Marik’s very recent take on IVC collapse and thank Scott for posting my vodcast on the topic. The discussion also included a very […]
[…] un peu d’écho, avec cette note sur la veine cave https://emcrit.org/isepsis/isepsis-vena-caval-ultrasonography-just-dont/ qui fait écho à l’analyse de The Bottom Line de l’étude […]
Hi Paul, Great article thank you. Can I please ask you what clinical tools or changes in patient presentation that you would use in a prehospital setting with access to ultrasound to determine the fluid responsiveness, particularly in septic patients?
Regards
Shane
Shane. Good question. Changes in carotid Doppler velocity with either a PLR or fluid bolus has been demonstrated to be a good indicator of fluid responsiveness. The carotid is easy to access and the technique is easy to learn. I think this would be a useful tool in the pre-hospital setting.
Thank you for your reply. Most of the current research I have found supports the changes in carotid Doppler velocity, but seems to only be in mechanically ventilated patients. Do you think it could be extrapolated to non-ventilated patients? Obviously in combination with good clinical judgement. I have tried to look at your post to see if I can find the answer but sorry I can’t hence the reply. Sorry if it’s taking up too much of your time. Thanks in advance
Share.. no sweat. You are right, most of the studies have been done in ventilated patients however we have used this technique with great success in non-ventilated patients; and I see no reason physiologic reason why it should no be helpful in the non-ventilated patient.
References
1. 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.
2. 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.
3. 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.
4. 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.
Im Jim, from Perú. Im trying to use the carotid volumen flow…so wich is better? These one or the Changes in carotid Doppler velocity? Both are easy to use…
Many have used peak velocity as it is somewhat easier to measure. However if you can measure flow as well I think it may be more accurate due to flow mediated vasodilatation. I would therefore recommend you measure both.
Dr. Marik,
What are your thoughts about using the NICOM after a passive leg raise for fluid responsiveness? Do you believe this is an acceptable approach or should carotid flow and/or LVOT VTI be utilized instead.
Thank you.
Brian
Dr. Marik,
What are your thoughts on NICOM for fluid responsiveness/passive leg raise? Do you think ultrasound for carotid flow and/or LVOT VTI is more appropriate?
Thank you.
Brian. Yes… A PLR coupled with NICOM is a very simple and practical method to determine fluid responsiveness with a high degree of accuracy. This can be done by the nursing staff with very little training. Carotid flow velocity or LVOT VTI are alternative techniques; however they require operators with expertise in this technology. Furthermore, in many patients it maybe difficult to obtain an adequate window to measure the VTI
Dear Dr Marik, thanks for the complete review of this topic.
Could you please give me the whole reference of the article you’re quoting about caval index distensibility? From de author Vignon et al., with 540 patients included.
https://www.google.co.in/url?sa=t&source=web&rct=j&url=http://criticalcarelondon.ca/wp-content/uploads/2016/11/Vignon-Echo-Fluid-Responsiveness.pdf&ved=2ahUKEwjJ0Y6ou_HYAhWJLY8KHQErDtMQFjAAegQIExAB&usg=AOvVaw3SN5biOblL_GyppQ-CPHUn
Vignon P. Am J Resp Crit Care Med 2017;195:1022-1032
Dude you don’t like to use IVC diameter neither CVP, so how do you assess fluid responsiveness, Sniff the pt ??
Haha good one but seriously, I think we have to go back to basics with clinical judgment. You can always use SVV but then again measuring that also has limitations.
Jem I agree. In the end one has to evaluate the patient at the bedside and not be bedazzled by technology. Recent critical care (and general medicine) studies have taught us that “Less may be More”. Don’t hurt the patient while you wait for the patient to recover. When unsure what to do regarding fluids give a small bolus of fluid (or diuretic as appropriate) and closely monitor the response. The change in the patients’ physiology is an important clue as to whether your interventions was helpful or harmful.
Mohoo (msn@msn.com) There is no place for unprofessional and rude comments on this Website. Multiple techniques have been scientifically evaluated and demonstrated to be excellent indices of fluid responsiveness. The PLR with an ROC of 0.94 is just one such technique.