Inferior Vena Cava may appear congested when it’s dilated without any respiratory variation collapsed with very small diameter through the respiratory cycle, or compliant and vary through respiratory cycle. But how IVC looks like depends on how the patientis breathing, spontaneouslyvs mechanically ventilated.

During spontaneous breathing, in inspiration there is a decrease in pleural pressure, partially transmitted to the heart chambers with a decrease in Right Atrial Pressureand increase in Venous Return (the lower the RAPthe easier the venous return). Because of this decrease in RAP there is a decrease in IVC transmural pressure the size (diameter) and a decrease in size of IVC.

To give numbers, a 40% variation in spontaneouslybreathingpatients is usually associated to preload responsiveness: patient will respond to fluids (but it does not mean that he needs fluids: gives only if associated hypotension/poor perfusion).

In patients with positive pressure ventilation physiology is completely reversed: you put positive pressure in the thorax, this is partially transmitted to the heart chambers whit an increase in RAP, an increase in IVC transmural pressure and in IVC diameter. We expect a dilated and non compliant Vena Cava due to the impeded venous return, collapsible vena cava is an abnormal finding. If you observe a compliant Vena Cava n a patient on MV, changing diameter with ventilation, actually increasing diameter with insufflation due to raised pressure in thorax impeding venous return and flattening in expiration with pressure release), this means that probablythis patient has volume in the veins that can be recruited. A > 12-18% variation in mechanically ventilated patientis usually associated to preload responsiveness(Feissel et al. 2004 http://bit.ly/2Cvm6Fp; Barbier et al. 2004 http://bit.ly/2Pb8R3p).

In patients with elevated Intra-Abdominal Pressure IVC is not interpretable anymore.

The endpoint of resuscitation is improve tissue perfusion, not to increase IVC diameter. The respiratory variations in large vessels just attest that there is some stressed volume that can be recruited: is vein collapses there is room to expand a little more and by increasing the stressed volume there is an high probability to increase the venous return and cardiac output if you think this in needed.And remember: IVC measurement really simple but not make the vena cava say what it can’t say.

Pictures from Cholley B talk at #LIVES2018

It was delightful listening to Paul Mayo deliver this excellent talk based on his clinical experience.

Critical care echocardiography is a different beast to the traditional “echo lab” approach favoured by cardiology. Our environment does not lend itself well to hour long studies per patient recording every measurement.

His unit adopts a flexible approach, deploying aspects of advanced echo as needed to answer specific clinical questions. Occasionally a full study will be performed. For quality control reasons, all their TOEs (TEEs) are full studies.

NYC is staffed by 10 attending and 6 “night owls”, all of whom are competent in general critical care ultrasound. 3 of the team are competent in advanced echo.

As an example of how they apply advanced skills, All shocked patients will get VTI to estimate stroke volume. Other measurements are used selectively such as:

• E/e’ to estimate filling pressures
• Bubble studies for hypoxemia
• Quantitative studies of valve function
• Precise measurements of RV function (PASP, PADP, PAMP, RV S’, PAT, TAPSE)
• Regional wall motion abnormality assessments
• serial echoes for dobutamine or nitric oxide trials

Images are saved, and relevant findings documented in notes (except TOEs which all get a ful, report). Interesting cases are discussed at a weekly meeting.

For those training in advanced CCE, Mayo recommends ALL views and ALL measurements are performed in a specific sequence, and images rejected if they are suboptimal. Not only does it upskill the user, it brings credibility to the field and reassures our cardiology and imaging colleagues.

These were certainly useful points that all of us in the critical care and imaging community should take note of.

Prof Vieillard-Baron delivered this lecture and began by pointing out a great overall review on the topic https://t.co/5TZsRZIZ12

Causes:

1: pulmonary embolism – management strategies here https://t.co/Cwc7drmG5z

• risk stratification by echo: https://t.co/GmDYz6T2yE
• Echo diagnostic criteria- McConnel’s sign, the 60/60 sign, RV ejection flow pattern (excellent 5 minute sono vid on this https://t.co/As4cgbM420)
• Occasionally you might see clot in transit!
• https://twitter.com/iceman_ex/status/911920877897502722

2: Acute myocardial infarction

3: Mechanical  ventilation – especially if a PFO is recanalised https://t.co/NwC6XPI91H

4: ARDS (https://t.co/pVj3GBSJnE)- here are some expert guidelines to manage haemodynamics https://t.co/VJjyQbbZnA

5: chronic RV failure- differentiate this from acute using RV wall thickness and the PASP (again, 5 minute sono has a wonderful example https://t.co/hmDtjSNZJ6)

If your RV is failing, Prof Vieillard-Baron recommends noradrenaline as it’s “magic for the RV”!