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
🧩 Part 3 – Why you usually can’t move one curve without the other
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So far, we’ve treated the cardiac and venous return curves as two lines that meet.
In theory, you can move one without the other – and sometimes that’s true.
But in physiology, they almost always move together – because they share the same inlet.
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Both curves hinge on the same gateway: the inlet to the heart.
That’s where Ivr – inlet impedance – lives.
Any change in relaxation, stiffness, or pericardial pressure alters Ivr, so both curves tend to shift together.
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Last time, we fixed the cardiac function curve.
Now let’s look at the other half of the story — venous return — and how the circulation really feeds the heart.
#FOAMed #MedX #physiology
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The venous return (VR) curve describes how blood flows into the heart for any steady state of the venous system.
It’s not about forcing RAP up or down — it shows the equilibrium between flow and pressure for a given system tone and volume.
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Mathematically:
VR = (Pms - RAP) / Ivr
• Pms = mean systemic filling pressure → “push” from stressed volume & venous tone
• Ivr = inlet impedance – how easily blood enters the heart (similar to Guyton’s RVR but dynamic, not fixed)
• RAP = dependent feedback pressure where inflow = outflow
🧵 The Cardiac Function Curve — why it misleads (Part 1) 1/ The cardiac function curve is one of the most recognisable images in physiology.
Unfortunately, it’s also one of the most misdrawn, mislabelled, and misunderstood.
Let’s redraw it — and see what it really tells us about the circulation.
#MedX #FOAMed #physiology
2/ Textbooks teach: ↑ filling pressure → ↑ output.
But that’s backwards.
The heart doesn’t decide flow — it matches whatever venous return delivers.
It’s a servo, not a suction pump.
3/ This cardiac function curve shows what the heart alone can do at different right-atrial pressures.
But cardiac output isn’t set by the heart in isolation — it’s where this curve meets the circulation’s ability to return blood.
We’ll come to that next time in part 2
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Some patients with severe venous congestion have almost no oedema — and that’s confusing at first.
It only starts to make sense once you unpack the physiology. 👇
Venous congestion ↑RAP → ↑venous pressure (Pv) → potentially ↑capillary pressure (Pc).
But the rise in Pc — and thus filtration — depends on arteriolar tone (Ra)
Pc = (Rv / (Ra + Rv)) * Pa + (Ra / (Ra + Rv)) * Pv
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If arterioles constrict (↑Ra), most of the pressure drop occurs before the capillary → Pc stays low and changes little even if Pv rises.
If they dilate (↓Ra), Pc shifts toward Pa → filtration ↑ → oedema.
But this neat number hides traps. It’s not “afterload,” it’s not pure “tone,” and sometimes it’s not even valid.
A thread on why systemic vascular resistance misleads — and when it still helps. 🧵 #MedX
2/ SVR isn’t measured.
It’s calculated from MAP, right atrial pressure, and CO.
That makes it a derived ratio — not a direct property of the circulation.
3/ Because it has “resistance” in the name, we imagine SVR = arteriolar tone.
It doesn’t.
It’s just arithmetic.
Decades of critical care RCTs.
Huge effort. Tens of thousands of patients.
Very few reproducible breakthroughs.
This is Part 3 of my series on why ICU trials fail — and why physiology must guide us.
2. Heterogeneity (noise, even in “real” diseases)
Even when the trial is valid, patients vary hugely:
– Baseline physiology, comorbidities, genetics
– Different illness phases (early vs late, compensated vs exhausted)
– Co-interventions (ventilation, sedation, antibiotics)
That means a treatment can help some, harm others.
The “needs bigger N” argument reflects the multi-causality of critical illness.
3. Timing & trajectory
Critical illness evolves dynamically.
The same drug may help early but harm late.
RCTs with broad enrolment windows average across very different biological states.
Example: steroids in ARDS → benefit if early/prolonged (DEXA-ARDS), harm if late (older ARDSNet trial).