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
🧵 Albumin in Critical Care: 70 Years, 700 Papers… Zero Benefit
1/ Albumin is the most studied fluid in critical care.
Decades of trials. Endless meta-analyses.
And yet – not a single clinically meaningful benefit.
Here’s why the entire theory collapses once you understand Extended Starling. 👇
2/ The old idea
We were all taught:
• albumin “pulls” fluid into vessels
• albumin “stays intravascular”
• albumin “treats oedema”
All based on the obsolete 19th-century Starling model.
3/ What Extended Starling actually says
Fluid exchange is governed by:
• Pc (capillary pressure)
• Pi (interstitial pressure)
• πc – πg (oncotic gradient)
• lymphatic return
The key oncotic gradient is across the glycocalyx – not between plasma and interstitium.
This destroys the logic that giving albumin should “draw fluid back.”
1️⃣
We can remove fluid at rates up to 12 mL/kg/h and blood pressure often holds.
That limit isn’t arbitrary – it comes from dialysis data showing steep rises in hypotension and mortality above it.
It marks the upper boundary of how fast plasma can be refilled from the interstitium and lymph 👇
2️⃣ The background
In most tissues, fluid filters out of capillaries and returns via the lymphatics.
At steady state, filtration ≈ lymph flow (~10 L/day ≈ 400 mL/h), so plasma and interstitial volumes stay constant.
This is the equilibrium that ultrafiltration later exploits.
3️⃣ What ultrafiltration actually does
Removing plasma water slightly lowers blood volume and triggers reflex arteriolar constriction (↑ Ra).
That drops capillary pressure (Pc), pushing the microcirculation left on the J-curve.
Filtration falls toward zero — you’ve effectively turned off the tap that was sending ~400 mL/h into the interstitium.
1️⃣We talk endlessly about “capillary leak” – but most of what we say about it is wrong.
Here’s what actually drives fluid movement across the microcirculation – and why Starling’s model needed an upgrade. A 🧵👇
2️⃣ The old picture
Starling (1896) imagined that filtration dominates early in the capillary and re-absorption later, where pressure is lower.
In most tissues, direct re-absorption almost never happens.
Capillary pressure (Pc) slightly exceeds oncotic pressure along the whole capillary, so filtration (Jv) predominates at both ends.
All that filtrate returns to the circulation through the lymphatics.
Fluid leaves the circulation continuously – and the lymphatics bring it back.
3️⃣ The extended Starling principle
Jv = Lp · S · ( (Pc − Pi) − σ · (πc − πg) )
• Pc – capillary hydrostatic pressure
• Pi – interstitial pressure
• πc – plasma oncotic pressure
• πg – oncotic pressure just beneath the glycocalyx (the effective gradient)
That thin, protein-free layer (πg ≈ 0) is what really opposes filtration.