Post holiday season, @ICUltrasonica, @wilkinsonjonny & I are back to take you through the most most critical clinical questions on #haemodynamics that ultrasound can answer
Aortic dissection is easily missed, carries a high mortality and should be on the differential of any patient with shock, abdo pain or chest pain. Contrary to popular belief the entire aorta can be imaged via transthoracic and abdominal ultrasound. Let’s start with some anatomy
Asc aorta:
Visualised from PLAX view with depth ⬇️ & probe tilted to focus on the root. Tilting superiorly, or moving up a rib space, may help. Examine the AV and look for a dissection flap. Measure the diameter 3-4cm from the AV. The root can also be seen from A5C & A3C views
Aortic arch:
Place the probe in the supra-sternal notch with the marker directed to 1 o’clock. Angle down to cut through a line between the right nipple and tip of left scapula.
Thoracic aorta:
From the PSAX view at MV level, tilting anteriorly and rotating anticlockwise will modify the view for the descending aorta.
It can also be visualised from a between a traditional A2C/A3C view (which we call the ‘apical 2.5’). Centre the descending aorta in the A4C view and rotate anticlockwise until probe cephalad/caudad in line with the aorta. Shout out to @sharonmkay for showing us these aorta views
Abdominal aorta:
Examine the aorta between the xiphisternum and umbilicus in long and short axis. (Bowel gas can get in the way)
Dissection features: 1. DILATATION
The anatomy cartoon above includes normal measurements. As a rule of thumb if the aorta is >4cm 3-4cm from the aortic valve then it is dilated. The aorta narrows as it continues & the descending aorta should not be >3cm.
Dilated root + flap:
2. DISSECTION FLAP
An intimal flap separates the true and false lumen which appears as a mobile linear structure moving independently of surrounding structures (in contrast to an artefact). Colour Doppler will demonstrate different flow patterns in the true and false lumens.
Dilatation and flap in A5C view
Flap seen in suprasternal view
Descending thoracic aorta flap from suprasternal view (source unknown)
3. Proximal involvement/extension.
This can disrupt the pericardium causing a pericardial effusion/tamponade, the aortic valve causing acute AR and the sinuses of valsalva (where the coronary arteries originate) causing ischaemia. See 2. dissection image above and note the LV fx
A FUSIC HD practitioner should regard thoracic aortic dissection as a rule-in, not rule-out, diagnosis. If suspected its associated features should be looked for. And vice versa. Have a low threshold for further imaging with CT or TOE.
oA FUSIC HD practitioner should regard h
Abdominal aorta
The AA should be examined between the xiphisternum and umbilicus in long and short axis. This will image it from the diaphragm to the iliac branches. It lies on the left hand side of the the IVC anterior to the spine. See pictures above
Most AAAs are infra-renal. US dilatation of the AA has high sensitivity so rupture can be ruled out. Ruling in is more challenging. US signs include aneurysm, thrombus, para-aortic collection and free abdominal fluid. Further evaluation with CT is required if clinically suspected
Guidelines for performing a complete haemodynamic exam can be found here bit.ly/3gxUvHh
Thanks for some great comments on this thread. Some nuance and further explanation is needed here.
Being ill activates the symp NS. I’m sure you have all noticed being tachy and having a bounding pulse when you have flu or are hungover! CO goes up to meet ⬆️ metabolic demand.
Sepsis of course is the same and can result in a ⬆️or ⬇️ cardiac output. The key factor is the balance between sepsis causing venoplegia (reducing Pms) and the sympathetic response trying to counter this (which increases Pms and HR).
If the sympathetic response wins, increasing Pms & HR, then a ⬆️CO and ⬇️SVR will result. Thanks to @PhilGuerci for the experimental sheep data.
Being sedated/anaesthetised blunts the sympathetic response. Here you will get reduced Pms and CO as in the data in my original thread
#haemodynamics #hemodynamics myths.
Myth 1.
'Sepsis causes low SVR and high stroke volume/CO'
This is a common misconception. Why? Because the moment a sick patient comes anywhere near a health care provider they get fluid boluses.
Animal studies show that in sepsis CO decreases (because of venous pooling / low Pms) and SVR increases. RAP was unchanged demonstrating this was not heart failure (but rather low Pms) causing reduced VR/CO. BP and CO were closely related. among others.jci.org/articles/view/…
In Q1 we saw how to measure stroke volume (SV). Q2 helps us manage someone with an inappropriately low SV. Pressors, fluids and inotropes are all treatment options. If If used correctly, they will ↑SV. If not, they won’t, and they may even be harmful.
Measuring VTI before and after each of these interventions will therefore easily show you if they have worked. But can we predict which one is likely to work before we give drugs or a drop of fluid? 1st, let’s go back to some physiology.
@iceman_ex@avkwong Really interesting study. Before I read it I assumed that 'physiological assessment' would be lots of fluid responsiveness assessment and then filling to an unresponsive (pathological) state. In fact a lot of ultrasound was used. And there was no difference in fluid administered
@iceman_ex@avkwong So why did US not help? Echo doesn't tell you whether there is hypovolaemia or not. A hyperdynamic heart is a feature of low venous return which is more often from venoplegia than hypovolaemia. Echo cannot distinguish between these.
@iceman_ex@avkwong Lung US shows if there is pulmonary oedema or not. You have to be significantly fluid overloaded to develop this though and its absence is definitely not a sign to give fluid.
Early in the outbreak it was commonly advised to aim for a -ve fluid balance
More recently a higher than expected occurrence of AKI and RRT has been observed prompting calls for a more liberal fluid strategy.
All these miss the point about the type of fluid being administered
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Hypovolaemia (low intravascular volume) should be avoided (AKI and other organ dysfunction).
Hypervolaemia (high intravascular volume) should be avoided (AKI via venous congestion, pulmonary oedema, R heart strain and other organ dysfunction)
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