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
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).
🧵 Part 2. Heterogeneity vs Colliders in Critical Care RCTs
1. The puzzle
Critical care RCTs keep failing.
The usual explanation?
“Patients are too heterogeneous.”
That’s partly true — but there’s a deeper problem.
Part 2 of a 3-thread series on why ICU trials fail and why physiology must guide us.
2. Heterogeneity (the usual alibi)
Heterogeneity = patients in the same trial differ in ways that matter:
– Age, comorbidities, severity
– Disease heterogeneity (e.g. pneumonia due to strep vs haemophilus)
– Different physiology
This makes treatment effect harder to see. Solution? Bigger trials, subgroups, precision medicine.
👉 RCT model still valid — just noisy.
3. Colliders (bias):
Colliders = when distinct diseases are grouped under one label (e.g. “sepsis”).
Pneumonia sepsis vs UTI sepsis may look the same at the bedside — but causes, trajectories, & treatment responses differ.
Unlike heterogeneity, this isn’t just noise — it’s bias.
👉 And that’s the deeper critique.
Decades of critical care research have produced few reproducible breakthroughs.
Maybe the problem isn’t our interventions — it’s that we reduce patients to syndromes, instead of treating them as individuals with distinct physiology.
2. The RCT problem
Critical care RCTs keep failing.
Sepsis and ARDS trials are the classic examples: huge effort, massive cost… yet most results are negative, inconsistent, or impossible to replicate.
3. What happens next?
Despite this, bundles of care get implemented.
If a patient meets sepsis thresholds, they may be given 30 ml/kg fluid as a default — even though their physiology may make this dangerous.
Thresholds create recipes, not treatments.
1/21
Acid–base interpretation often feels like a maze.
But there’s a simple way to make sense of it at the bedside.
It starts with pH, strong ions, and base excess.
2/21
First: what is pH?
pH = the concentration of hydrogen ions, which come from water splitting into H⁺ and OH⁻.
Anything that changes how much water dissociates changes pH.
3/21
Ions drive this process.
👉 Strong ions (Na⁺, K⁺, Cl⁻, lactate⁻) fully dissociate, their charges are fixed.
👉 Weak acids (albumin, phosphate, bicarbonate) only partly dissociate and buffer H⁺.
1/ Shock isn’t “give fluids, then pressors, then inotropes.”
That recipe misses the physiology.
Here’s how to manage shock properly: 🧵
#MedX #haemodynamics
2/ First, rule out mechanical causes (tamponade, tension PTX, massive PE, acute valve rupture, etc). These need specific fixes.
3/ Once you’ve ruled out mechanical causes, shock comes down to two mechanisms:
• The pump fails (heart can’t move blood forward)
• The pipes fail (low venular pressure → ↓mean systemic pressure (Pms) → ↓venous return)
That’s the physiology behind almost every case.