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
1/ In our last thread, we explored how vessels can collapse when MAP falls below a threshold — the Critical Closing Pressure (CCP) — creating a vascular choke point.
But there’s a common misunderstanding we need to clear up 🧵👇
#MedX #Physiology #Haemodynamics
2/ The concept of the vascular waterfall helps explain this:
When CCP rises above venous pressure, blood flow can cease completely — even if a pressure gradient still exists.
Why “waterfall”? Because flow is no longer influenced by the pressure downstream.
3/ Think of a real waterfall:
💧 The height of the pool at the bottom (CVP) doesn’t control whether water flows over the edge.
🌊 Flow is governed by the pressure at the lip of the cliff — that’s your CCP.
If pressure at the top drops below the lip, flow stops — regardless of downstream pressure.
🧵 What is Critical Closing Pressure — and why does it matter for perfusion?
A thread to clear up one of the most misused and misunderstood ideas in circulatory physiology.
👇
1.
We talk a lot about MAP, CVP, and perfusion pressure.
But there’s a hidden threshold that can choke flow completely — even when there’s still a gradient.
It’s called Critical Closing Pressure (CCP).
And it’s time to make sense of it.
2. What is CCP?
CCP is the arterial pressure below which a vessel collapses and flow stops, even if CVP is lower.
It’s not theoretical. It’s real, measurable, and clinically important — when the conditions are right.
1/ Shock is complex. But our tools are often simplistic.
This paper proposes a new model:
🩸 Four circulatory interfaces that must stay coupled to maintain perfusion.
Uncouple any one — and shock worsens.
#Shock #MedX #FOAMcc
Here’s the framework.
🔗 doi.org/10.3390/jpm150…
2/ 🔧 The model outlines 4 key interfaces: 1. LV to systemic arterial 2. Arteriolar to capillary 3. Capillary to venular 4. RV to pulmonary arterial
Each can be assessed. Each can fail. And each demands tailored therapy.
3/ Interface I: LV–Arterial Coupling
The heart and arteries must be matched – contractility (Ees) and afterload (Ea).
Uncoupling?
– Hyperdynamic sepsis can mask LV dysfunction
– Pressors unmask it
– LVEF drops despite “normal” MAP
🔍 LVEF is the best bedside tool here – not for contractility, but because it reflects load-dependent coupling.
🧵 Starling’s Law: Misunderstood, Misapplied, and Still Misleading
1
🚨 “Starling’s Law explains how the heart increases cardiac output.”
You’ve probably heard this a thousand times.
But it’s wrong.
Or at least - very incomplete.
Let’s fix it.
Because this matters - for heart failure, fluids, vasopressors, inotropes, afterload, and how we think about the whole system.
2
🫀 Textbook Starling curves show:
Preload (RAP or EDV) on the x-axis
Cardiac output on the y-axis
Upward shifts with “more inotropy” or “less afterload”
❌ But that’s not how the system really works.
Because in a real circulation, the system sets flow - not the heart.
3
In reality:
• Flow is determined by Pms − RAP / Rvr
• The system sets mean systemic pressure - Pms (by venous volume and elastance)
• The heart’s job is to accept the return
• CO ≈ venous return (unless the heart starts to fail)
1/ Most people think the heart drives circulation.
But what if that’s backwards?
Anderson’s model flips the whole idea of cardiac output on its head — and it changes how you think about fluid, flow, and failure.
🧵👇
#physiology #FOAMed #MedTwitter #criticalCare #cardiacOutput
2/ 🚿The system sets the flow based on metabolic need.
It adjusts vascular tone and volume to change Pms (mean systemic pressure) and venous return.
The heart simply ejects what arrives — unless it fails.
3/ 🫀The heart doesn’t suck.
It doesn’t pull blood in.
It’s not a centrifugal pump or piston.
It’s more like a bladder.
It passively fills — and just empties what shows up.