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Husband. Intensivist at St Bartholomew’s Hospital, London. Ultrascoundrel. U.K. Intensive Care Society Council. All about the 
#foamed and #foamcc.
@load_dependent brilliant thread as ever, my friend.
- Echo cannot differentiate between venoplegia and true hypovolemia as cause of low preload.
- Look beyond the heart for signs of congestion!
3/fin
- Normal values make no sense in the critical ill as they depend on normal load conditions and heart rate.
- Change in values over time is more relevant than absolute values.
- Beware that tamponade behaves differently in positive pressure ventilation (E-wave variation decreases? Rather than increases)
- If you really need to know CVP or PCWP, measure them invasively, echo is a wild guess.
- A combination of cardiac index, SVR and EF is very informative 2/
I did a talk for cardiologists about #criticalcareecho, emphasising the difference between outpstient/normal data and the critical ill. Supeisingly well recieved and I’ll reiterate my main points:
- Most important use for echo in critical illness is differentiating shock types, and detecting “black swan” conditions like LVOT obstruction and acute valvular pathologies
- Always combine echo with clinical findings.
1/
#echocardiography #CriticalCare #physiology
@load_dependent great thread Lars!
Interesting review of diastolic function grading in critically ill patients, basically arguing for left atrial strain. Some comments follow : https://onlinelibrary.wiley.com/doi/10.1111/echo.15773 #echocardiography #CriticalCare #cardiology
What we need in #criticalcareechocardiography is less extrapolation from outpatient populations under normal loading conditions, and more studies evaluating effect in individuals of changing load conditions on these parameteres and how these parameteres are able to track changes in loading conditions and distolic function. My hunch is that as with fluid responsiveness, we will discover that static parameters are useless, dynamic are useful.
@load_dependent watch this space for some interesting data around LA size…
Much the same applies to left atrial strain. It's for the most part a composite of left atrial size, and left ventricular long axis function. Left atrial size does not vary much acutely, while left ventricular long axis function is as discussed generally reduced by all unfavourable loading conditions including high afterload and low preload.
A classic low preload, low afterload, high inotropy septic circulation will increase EF, but since GLS is considerably more sensitive to preload and heart rate, it will rather be decreased just as VTI and stroke volume will. This explains to a large degree I think the linearity for GLS, vs the non-linearity for EF. It does not mean GLS is more usefull or informative!