Cardiac Output

After a straightforward valve operation, TAPSE is twelve millimetres — well under the transthoracic normal. But the fractional area change is 40 per cent, the 3D ejection fraction is 48 per cent, and the lactate is falling. Which number is lying?
This is part two of two on the right ventricle on transoesophageal echo, following the right ventricle chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. It's about measurement: which numbers to trust, when, and why bypass changes the way the right ventricle contracts — longitudinal shortening falls and circumferential contraction rises, for up to a year.
We go through each systolic measure: TAPSE and the TOE alignment problem (and anatomical M-mode), S-prime and why transthoracic cut-offs don't transfer, fractional area change, 3D ejection fraction, speckle-tracking strain, and the myocardial performance index — with normal values and pitfalls for each.
Then diastolic function — E, A, E-prime and deceleration time — and how E over E-prime unmasks pseudonormal filling. Finally, congestion beyond the heart: the A, S, V and D waves of hepatic vein flow and how they change as the right ventricle fails, portal vein pulsatility, intrarenal venous flow and the resistive index, and why IVC collapse doesn't translate to TOE.
We finish with Calum sorting every measure into traffic lights: trust it, use with caution, or leave it.
Chapters
(00:00) Cold open — TAPSE says failing, FAC says fine
(01:05) Geometric and non-geometric measures
(01:25) TAPSE on TOE
(02:40) Tissue Doppler S-prime
(03:15) Fractional area change
(03:55) 3D ejection fraction
(04:50) Strain and speckle tracking
(05:45) Myocardial performance index
(06:35) What to trust after bypass
(06:55) Diastolic function
(07:55) Relaxation, pseudonormal and restrictive filling
(08:45) Congestion beyond the heart
(09:05) Hepatic vein Doppler
(10:05) Portal vein pulsatility
(10:30) Renal venous flow
(10:55) The IVC on TOE
(11:10) Traffic lights
Key takeaways
After bypass, RV longitudinal function falls and circumferential contraction rises for up to a year — interpret TAPSE and S′ with caution and lean on global measures
TAPSE (normal >16 mm on TTE) is underestimated in the ME four-chamber view unless anatomical M-mode or the deep transgastric RV inflow view is used
S′ (TTE normal ≥9.5 cm/s pulsed-wave, ≥6.0 cm/s colour TDI) has not been validated in TOE views
FAC = (RVEDA − RVESA) ÷ RVEDA; below 35% is abnormal; angle-independent, includes trabeculations, inflow portion only
3D RVEF above 45% is normal; needs ≥25 Hz, often multi-beat ECG-gated acquisition; may underestimate volumes
RV free wall strain more negative than −20% is normal; speckle tracking needs good images and frame rates above ~40/s
MPI = (IVCT + IVRT) ÷ ET; normal <0.43 (PW) or <0.54 (TDI); unreliable with arrhythmia or high RAP
Diastology: E/A 0.8–2.1, E′ 0.08–0.20 m/s, E/E′ 2–6, deceleration time 120–200 ms; E/E′ >6 with a normal E/A suggests pseudonormalisation
Restrictive RV filling: E/A >2.1 with a deceleration time <120 ms
Hepatic vein flow as the RV fails: exaggerated A-wave, blunted then reversed S-wave, relatively larger D-wave
Portal flow becomes pulsatile with congestion (pulsatility index normally <0.5); intrarenal venous flow becomes pulsatile and the resistive index rises (normal <0.7)
IVC size and collapsibility are not validated with TOE or positive-pressure ventilation
References / further reading
The right ventricle (Chapter 14). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686
Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography. J Am Soc Echocardiogr 2010; 23: 685–713
Silverton NA, Gebhardt BR, Maslow A. The intraoperative assessment of right ventricular function during cardiac surgery. J Cardiothorac Vasc Anesth 2022; 36: 3904–15
Denault AY, Haddad F, Jacobsohn E, Deschamps A. Perioperative right ventricular dysfunction. Curr Opin Anaesthesiol 2013; 26: 71–81
Rola P, Miralles-Aguiar F, Argaiz E, et al. Clinical applications of the venous excess ultrasound (VExUS) score: conceptual review and case series. Ultrasound J 2021; 13: 32
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
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This podcast is for medical education for healthcare professionals. It is not clinical advice.

In the 1940s, researchers burned away most of the right ventricular free wall in dogs, and the venous pressure barely moved. For decades, the right ventricle was treated as a passive conduit. Nobody who has watched one fail coming off bypass believes that now.
This is part one of two on the right ventricle on transoesophageal echo, built around the right ventricle chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. Severe acute right ventricular failure after cardiac surgery is uncommon, but when it's refractory, hospital mortality is between 22 and 90 per cent.
We cover the anatomy — three parts, four walls, a 55-degree angle between inflow and outflow, and a peristaltic contraction with three distinct movements — and how much the left ventricle contributes. Then the blood supply wall by wall, and why air in the right coronary is the commonest cause of sudden right ventricular failure as you come off bypass.
Then the physiology: why the right ventricle tolerates gradual rises in afterload but not sudden ones, and why more fluid can lower the cardiac output of a failing right ventricle. Then the six TOE views, normal sizes for the inflow, outflow and wall, and the rule that right ventricular enlargement should never go unexplained.
Finally, reading the septum — volume overload versus pressure overload, the eccentricity index, and the interatrial septum — before Calum tests himself with six true-or-false statements. Part two covers measuring function and seeing congestion beyond the heart.
Chapters
(00:00) Cold open — the passive conduit
(01:00) Who's at risk
(01:20) Anatomy: three parts and four walls
(02:05) Recognising the right ventricle
(02:30) How it contracts
(03:10) Blood supply, wall by wall
(03:40) Air in the right coronary
(04:10) Other causes after bypass
(04:25) Physiology and afterload
(05:00) Volume, Frank–Starling and the septum
(05:40) The TOE views
(07:15) Measuring size
(08:05) Wall thickness and unexplained enlargement
(08:45) Reading the septum
(09:25) The eccentricity index
(09:55) The interatrial septum
(10:15) True or false
Key takeaways
Severe acute RV failure after cardiotomy is around 0.1%, but refractory RV failure carries 22–90% hospital mortality
Highest risk: pre-existing RV dysfunction, severe pulmonary hypertension, heart or lung transplant, and LVAD implantation
The RV has an inlet, an apical trabecular part and an infundibulum; four walls (free/lateral, anterior, inferior, infundibulum); inflow and outflow at about 55°
Contraction is peristaltic, from apex to infundibulum, with three movements: free wall inwards, base towards apex, and traction from LV contraction — the LV contributes up to 40% of RV pressure
Blood supply: lateral wall from the RCA alone (acute marginals); anterior wall and infundibulum from RCA and LAD; inferior wall and posterior third of the septum from the PDA
Air embolism to the RCA or RV grafts is the commonest cause of acute RV dysfunction when weaning from bypass
The RV tolerates gradual increases in afterload but decompensates with sudden ones; chronic pressure overload causes hypertrophy and a D-shaped LV in systole
Excess volume dilates the RV, shifts the septum left, impairs LV filling and worsens tricuspid regurgitation
Abnormal sizes: basal diameter >41 mm, mid >35 mm, proximal RVOT >35 mm, distal RVOT >27 mm, free wall >5 mm
RV enlargement should never go unexplained — exclude a shunt or other primary cause before blaming the LV
Volume overload: septal flattening in diastole only; pressure overload: in systole and diastole; a systolic eccentricity index >1.08 predicts pulmonary hypertension
A leftward shift of the interatrial septum suggests raised right atrial pressure
References / further reading
The right ventricle (Chapter 14). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686
Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography. J Am Soc Echocardiogr 2010; 23: 685–713
Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation 2008; 117: 1436–48
Crystal GJ, Pagel PS. Right ventricular perfusion: physiology and clinical implications. Anesthesiology 2018; 128: 202–18
Silverton NA, Gebhardt BR, Maslow A. The intraoperative assessment of right ventricular function during cardiac surgery. J Cardiothorac Vasc Anesth 2022; 36: 3904–15
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

A patient comes for coronary bypass. Last month's echo called the mitral regurgitation severe. After induction, it looks moderate. The surgeon asks: "Do I need to touch the valve?"
This is part two of two on the mitral valve on transoesophageal echo, following the mitral valve chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. It's all about severity — and the rule that runs through it: never trust one number.
For regurgitation, we start with why general anaesthesia can make it look a whole grade better, and how to restore awake loading before you grade. Then the clues from the rest of the heart, including why a "normal" ejection fraction in severe regurgitation isn't normal. Then each method in turn: colour jet area and why wall-hugging jets are severe until proven otherwise; vena contracta width and three-D vena contracta area; PISA, the effective regurgitant orifice area and regurgitant volume, the radius-squared-over-two shortcut and its pitfalls; and pulmonary vein flow, continuous-wave density and the E-wave. We cover timing within systole, slit-like orifices, and the long argument over thresholds for secondary regurgitation.
For stenosis: rheumatic versus calcific disease, commissural fusion and the hockey stick, the left atrial appendage and spontaneous echo contrast; then mean gradient, valve area and the A-to-D staging, pressure half-time and what distorts it, and why 3D planimetry is the preferred method.
We finish by writing the report the surgeon in the cold open actually needs.
Chapters
(00:00) Cold open — severe on the ward, moderate in theatre
(00:50) Grading under anaesthesia
(01:40) What the rest of the heart tells you
(02:20) Colour jet area and wall-hugging jets
(03:05) Vena contracta width
(04:05) Vena contracta area in 3D
(04:40) PISA, EROA and regurgitant volume
(06:05) The PISA shortcut
(06:45) PISA pitfalls
(07:25) Pulmonary veins, CW density and the E-wave
(08:25) Timing in systole and orifice shape
(09:10) Secondary regurgitation and its thresholds
(09:55) Mitral stenosis: causes
(10:20) Recognising the rheumatic valve
(11:20) Grading stenosis and A-to-D staging
(12:15) Mean gradient
(12:30) Pressure half-time
(13:35) Planimetry in 3D
(14:00) PISA and continuity in stenosis
(14:25) Writing the report
Key takeaways
General anaesthesia can make MR look a whole grade less severe — grade awake if possible, or restore awake loading first
Use several methods together: flow convergence, vena contracta, jet size and downstream effects
In severe MR the EF should be supranormal; a "normal" EF may hide dysfunction — report it "in the presence of severe MR"
Jet area under 20% of the LA suggests mild and over 40% severe, but it's unreliable — and wall-hugging jets are severe until proven otherwise
Vena contracta width in the mid-oesophageal long axis: under 3 mm mild, 7 mm or more severe; not valid with multiple jets
3D vena contracta area makes no assumption about orifice shape and can sum multiple jets
PISA: EROA = 2πr² × Nyquist ÷ peak MR velocity; EROA under 0.2 cm² mild, over 0.4 cm² (regurgitant volume ≥60 mL) severe
Shortcut: at a Nyquist of 40 cm/s and a 5 m/s jet, EROA ≈ r²/2 — a radius of 1 cm or more suggests severe (not valid with a poor LV)
Systolic flow reversal in two or more pulmonary veins is specific for severe MR; an A-dominant mitral inflow argues against it
Secondary MR is load-dependent, often slit-like and underestimated — the best time to grade it is preoperatively, awake
Rheumatic MS: commissural fusion, thickened tips, chordal involvement and diastolic doming; check the LA appendage for thrombus
MS severity: mild >2.5 cm² and mean gradient <5 mmHg; moderate 1.6–2.5 cm² and 5–9 mmHg; severe <1.5 cm² and >10 mmHg — report the heart rate
Pressure half-time: MVA ≈ 220 ÷ PHT; distorted by anything that changes LV filling, and unreliable straight after repair or valvotomy
3D planimetry at the leaflet tips is the preferred way to measure mitral valve area
References / further reading
The mitral valve (Chapter 8). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686
Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation. J Am Soc Echocardiogr 2017; 30: 303–71
Pandian NG, Kim JK, Arias-Godinez JA, et al. Recommendations for the use of echocardiography in the evaluation of rheumatic heart disease: a report from the American Society of Echocardiography. J Am Soc Echocardiogr 2023; 36: 3–28
Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease. Circulation 2021; 143: e72–e227
Grayburn PA, Chandrashekhar YS. Functional mitral regurgitation: more questions than answers. JACC Cardiovasc Imaging 2021; 14: 711–14
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

The cross-clamp is on, the atrium is open, and the surgeon looks up over the drapes: "Is it P2 or P3 — and is the anterior leaflet involved?" Everyone turns to the person with the TOE probe.
This is part one of two on the mitral valve on transoesophageal echo, built around the mitral valve chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. We start with why the mitral valve is such a good TOE valve, then the anatomy as a whole apparatus: the saddle-shaped annulus and its two axes, the leaflets and the Carpentier segments, coaptation length, the papillary muscles and their blood supply, and the chordae.
Then orientation — the anatomical, surgeon's and TOE views — and which segments you see in each standard view, why the commissural view misleads you about jet width, and why the four- and two-chamber views cut the valve obliquely. We cover axial imaging along the mitral–apex axis, live 3D, multiplanar reconstruction, and how to spot and eliminate parallax.
Finally, mechanism: fibroelastic deficiency versus Barlow disease and mitral annular disjunction; asymmetric and symmetric tethering in secondary regurgitation, with tenting height and area; atrial functional regurgitation; rheumatic disease, endocarditis, clefts, papillary muscle rupture and systolic anterior motion; and the Carpentier classification, prolapse versus flail, and what the jet direction tells you.
We finish at the probe: you call out the movements, and Calum names the segments. Part two covers grading regurgitation and stenosis.
Chapters
(00:00) Cold open — P2 or P3?
(00:55) Why the mitral valve suits TOE
(01:30) The annulus: a riding saddle
(02:35) Leaflets, segments and coaptation
(04:00) Papillary muscles and their blood supply
(04:45) The chordae
(05:15) Orientation and the standard views
(07:10) Four- and two-chamber views, and landmarks
(08:20) Axial imaging along the mitral–apex axis
(09:35) 3D, multiplanar reconstruction and parallax
(10:35) Degenerative disease: FED, Barlow and MAD
(11:50) Secondary regurgitation and tethering
(13:10) Atrial functional regurgitation
(13:30) Rheumatic, endocarditis, clefts and papillary rupture
(14:10) Systolic anterior motion
(14:40) Carpentier, prolapse versus flail, and jet direction
(16:05) Measuring the annulus
(16:45) Driving the probe
Key takeaways
Think of the mitral valve as an apparatus: annulus, leaflets, chordae, papillary muscles and the LV wall
The annulus is saddle-shaped, with a short, high anteroposterior axis and a long, low commissural axis; systolic contraction reduces its area by about a quarter
The posterior leaflet has twice the annular attachment but half the base-to-tip length of the anterior leaflet; normal coaptation length is 8–10 mm
The posteromedial papillary muscle usually depends on the right coronary artery alone, so its ischaemic rupture is far more common
Mid-oesophageal long axis: P2 left, A2 right, perpendicular to coaptation — use it for the AP diameter and the vena contracta
Mid-oesophageal commissural view: P3, A2, P1 — along the coaptation line, so jets look wider; don't measure the vena contracta here
Four- and two-chamber views cut the valve obliquely; don't use them for annular dimensions, leaflet lengths or the vena contracta
Axial imaging along the mitral–apex axis, or live and 3D multiplanar imaging, makes segment identification reliable — check for parallax
Fibroelastic deficiency: older, short history, single ruptured chord (often P2); Barlow: younger, long history, multisegment billowing, large annulus, often MAD
Inferior infarction causes asymmetric posterior tethering with a posterior jet; global remodelling causes symmetric tethering with a central jet; tenting height >1.0 cm or area >1.6 cm² is severe
Carpentier: type I normal motion, type II excessive (prolapse or flail), type IIIa restricted in diastole and systole, type IIIb restricted in systole
Prolapse and flail send the jet away from the diseased leaflet; restriction sends it towards it
SAM: fill, slow the heart, give a vasoconstrictor and stop inotropes
References / further reading
The mitral valve (Chapter 8). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686
Sidebotham DA, Allen SJ, Gerber IL, Fayers T. Intraoperative transesophageal echocardiography for surgical repair of mitral regurgitation. J Am Soc Echocardiogr 2014; 27: 345–66
Drake DH, Zimmerman KG, Hepner AM, Nichols CD. Echo-guided mitral repair. Circ Cardiovasc Imaging 2014; 7: 132–41
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

"Anaesthetist to the cath lab. Primary PCI, five minutes." Then the pause, while everyone waits to hear whether the patient is self-ventilating or intubated.
This episode is about anaesthesia for primary PCI — one of the few places where you're surrounded by people and still somehow on your own. We cover the range of patients the call can mean, from mid-arrest on a mechanical compression device to the agitated patient trying to climb off the table, and why the walk to the lab is the time to make your plan.
Then the room itself: why the cath lab isn't built for anaesthetists, why you and your assistant may be the only people thinking about the airway, and why help has to be asked for by name. What to do as you arrive — lead on before you go through the door, read the room, and ask what's needed. How to read the cardiology arterial trace when it has no alarms and a strange scale, and how to find and use the patient's access.
The central decision is the airway: if you've been called and you're not sure, intubate, and say so out loud so the room can stop for you. We cover gentle induction in a failing heart, getting a femoral central line from the cardiologist before the gloves come off, why not to delay the case for your own arterial line or keep the radial sheath, and careful fluids.
Finally, spotting cardiogenic shock early with the SCAI stages, voicing it, and escalating to mechanical support in time — then packaging the patient properly for intensive care. We finish with the walk to the lab: the plan to have in your head before you open the door.
Chapters
(00:00) Cold open — the bleep
(00:40) Who could be waiting for you
(01:40) Assessing the patient on arrival
(02:25) The cath lab: a room not built for us
(04:05) Lead on, read the room, ask what's needed
(05:10) Reading the cardiology monitoring
(06:05) Finding and using access
(06:40) To intubate or not
(08:10) Central access and fluids
(09:10) Arterial lines and radial sheaths
(10:20) Spotting cardiogenic shock
(11:20) Packaging for intensive care
(12:10) The walk to the lab
Key takeaways
The call can mean anything from mid-arrest to combative — use the walk to the lab to plan for each
On arrival: quick A to E, including supraglottic airways, aspiration, pulmonary oedema, shock and what drugs have already been given
Everyone else is focused on the artery; ask for help specifically, by name and task
Wear lead before you go through the door, read the room, introduce yourself and ask what's needed
Learn to read the cardiology arterial trace — scale, interruptions and no alarms — and tell the room you're watching it
Find the cannula, bring an extension to you, use a low-volume line, and close infusions after boluses
If you've been called and you're unsure, intubate — announce it so screening stops and the C-arm moves
Induce gently with a combination of agents, with a vasopressor drawn up first
Ask the cardiologist for a femoral central line; remind them before the gloves come off
Don't delay the case for your own arterial line, and don't keep a large radial sheath for monitoring
Use the SCAI shock stages, say "cardiogenic shock" out loud, and escalate to mechanical support early
Package the patient before leaving: arterial line, catheter, nasogastric tube, infusions, and an intensive care bed ready
References / further reading
Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv 2019; 94: 29–37
Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update: a review and incorporation of validation studies. J Am Coll Cardiol 2022; 79: 933–46
Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J 2023; 44: 3720–826
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

In carcinoid syndrome, you must never give adrenaline. Most of us were taught that — but it comes from decades-old experiments in end-stage patients who had never been near octreotide. So does the rule still stand?
This episode is carcinoid heart disease, from the tumour to intensive care. We start with neuroendocrine tumours and carcinoid syndrome, why the syndrome usually needs liver metastases, and why serotonin damages the tricuspid and pulmonary valves while the left heart is usually spared — and what it means when it isn't. Then the echo picture, why this disease progresses so much faster than other right-sided valve disease, how patients are screened and followed up, and what medical therapy can and can't do.
Then surgery: who should have it, why the cancer has to be under control first, the risk factors (including a deceptively low creatinine in sarcopenic patients), and the nutritional problems that come with the disease. We spend time on the right ventricle that looks fine with free tricuspid regurgitation and then fails once the valve works, and on how stress right heart catheterisation can help predict it.
In theatre: octreotide and what it really does, whether catecholamines are as dangerous as we were taught, what a carcinoid crisis looks like under the drapes, and the limited role of mechanical support. Then intensive care — the right ventricle, acute kidney injury, mesenteric ischaemia, heart block and how to avoid it — and where the field is heading, from transcatheter valves to liver transplantation.
We finish with a handover to the night team: everything you need to know about a carcinoid valve patient on day one.
Chapters
(00:00) Cold open — never give adrenaline?
(01:05) Neuroendocrine tumours and carcinoid syndrome
(02:40) What carcinoid heart disease is — and why it's right-sided
(03:50) The echo picture and how fast it progresses
(04:35) Screening and follow-up
(05:15) Medical treatment
(06:10) Nutrition and frailty
(07:00) Who should have surgery
(07:55) The right ventricle problem
(09:00) Preoperative assessment
(10:00) Octreotide
(10:50) Catecholamines: is adrenaline really forbidden?
(11:45) Carcinoid crisis
(13:00) Mechanical support
(13:35) The anaesthetic
(14:05) Intensive care: kidneys, gut and heart block
(16:10) Where the field is heading
(16:40) The handover
Key takeaways
Carcinoid syndrome usually needs liver metastases: their secretions bypass hepatic breakdown and reach the systemic circulation
Carcinoid heart disease is a paraneoplastic effect of serotonin and other mediators, not tumour in the heart — leaflets thicken, retract and fix open
It is classically tricuspid and pulmonary; left-sided involvement should prompt a search for a shunt, lung metastases or an ovarian primary — or other valve disease
It progresses quickly; screen with NT-proBNP and echo, never discharge from follow-up, and refer before the right ventricle fails
Medical therapy controls the syndrome and the fluid, but cannot reverse valve damage; big diuretic doses are common, before and after surgery
Malnutrition, niacin and vitamin D deficiency and pancreatic insufficiency are common; weight can hide muscle loss behind oedema
Operate only when the cancer is controlled; age over 70, frailty, renal impairment and complexity raise the risk
Free TR unloads the right ventricle — a competent valve can unmask failure; stress right heart catheterisation helps but isn't foolproof
Check for a PFO with a bubble study: it should be closed, and right-to-left shunting can cause hypoxia at induction
With octreotide on board, catecholamines don't appear to worsen outcomes; a small dilute adrenaline test dose is one cautious approach
Carcinoid crisis behaves like distributive shock: octreotide, fluid and early vasopressors
Watch for AKI, mesenteric ischaemia and heart block; extubate early, use depth-of-anaesthesia monitoring, and mobilise and feed early
References / further reading
Davar J, Connolly HM, Caplin ME, et al. Diagnosing and managing carcinoid heart disease in patients with neuroendocrine tumors: an expert statement. J Am Coll Cardiol 2017; 69: 1288–304
Grozinsky-Glasberg S, Davar J, Hofland J, et al. European Neuroendocrine Tumor Society (ENETS) 2022 guidance paper for carcinoid syndrome and carcinoid heart disease. J Neuroendocrinol 2022; 34: e13146
Connolly HM, Schaff HV, Abel MD, et al. Early and late outcomes of surgical treatment in carcinoid heart disease. J Am Coll Cardiol 2015; 66: 2189–96
Condron ME, Pommier SJ, Pommier RF. Continuous infusion of octreotide combined with perioperative octreotide bolus does not prevent intraoperative carcinoid crisis. Surgery 2016; 159: 358–65
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

Sixty-five per cent of patients on standard-dose heparin on ECMO had a severe bleed. Eleven per cent had a severe clot. And the heparin is there to prevent the eleven.
This is a journal club on RATE, published in The Lancet in July 2026: the first adequately powered randomised trial of anticoagulation intensity on ECMO. Three hundred and thirty adults on veno-venous or veno-arterial ECMO across seven Dutch intensive care units were randomised to standard-dose unfractionated heparin (APTT 2–2.5 times baseline), low-dose unfractionated heparin (1.5–2 times baseline) or therapeutic subcutaneous low-molecular-weight heparin.
We go through the question, the methods, the non-inferiority margin and what it actually means, and the results: both lower-intensity strategies were non-inferior, with no increase in thrombosis, no extra oxygenator changes, and a consistent but non-significant lean towards less bleeding and fewer deaths.
Then the critique — a composite endpoint dominated by death and bleeding, wide confidence intervals, a narrow definition of thrombosis, unstandardised APTT reagents, two thirds of ECMO patients never enrolled, and the practical problems with subcutaneous low-molecular-weight heparin in shocked patients — and the strengths.
Finally, what it means for us. Our unit already runs heparin at very low doses and reserves full anticoagulation for a specific indication such as pulmonary embolism; ECMO on its own isn't one. RATE draws the same line. And the practical point every resident should take away: blood products go through a peripheral drip, never the central line, because the oxygenator is downstream.
Chapters
(00:00) Cold open — sixty-five against eleven
(00:50) Why the standard target was never tested
(02:05) Trial design and patients
(02:30) Exclusions — and what they tell you
(03:00) The three arms
(04:00) The composite outcome
(04:45) Statistics and the non-inferiority margin
(05:40) Who was enrolled
(06:30) Did the arms separate?
(07:30) Primary outcome
(08:00) Bleeding, thrombosis and mortality
(08:50) Oxygenators and transfusion
(09:15) Crossovers, tracheostomy and subgroups
(09:55) Cost
(10:10) Critique
(12:10) Strengths
(12:30) What it means for our practice
(13:20) Blood products: peripheral, not central
(14:15) Wider implications and anti-Xa targets
(14:45) Three rules
Key takeaways
The standard ECMO target — UFH to an APTT of 2–2.5 times baseline (about 60–75 s) — had never been tested in an adequately powered randomised trial
RATE: 330 adults, VV and VA ECMO, seven Dutch ICUs; standard-dose UFH vs low-dose UFH (1.5–2 times baseline, about 45–60 s) vs therapeutic subcutaneous LMWH
Primary composite (severe bleeding, severe thromboembolism, 6-month mortality): 81% vs 72% vs 75% — both lower-intensity strategies non-inferior
Severe bleeding 65% vs 58% vs 59%; severe thromboembolism 11% vs 10% vs 9%; 6-month mortality 50% vs 42% vs 44% — all non-significant
No increase in oxygenator changes or transfusion with lower-intensity anticoagulation
Non-inferior is not superior: the confidence intervals are wide, and subgroup signals are hypothesis-generating only
Thrombosis was probably undercounted, APTT reagents weren't standardised, and most ECMO patients in the participating units weren't enrolled
Subcutaneous LMWH is less predictable in shocked, oedematous patients, accumulates in renal failure and can't be switched off quickly
ECMO on its own is not an indication for full anticoagulation — reserve that for a specific indication such as PE, a mechanical mitral valve or intracardiac thrombus
Give blood products through a peripheral drip, not the central line, to avoid sending a bolus of clotting factors straight onto the oxygenator
References / further reading
van Minnen O, Oude Lansink-Hartgring A, van Amstel RBE, et al. Standard-dose unfractionated heparin versus low-dose unfractionated heparin and low-molecular-weight heparin in extracorporeal life support (RATE): an open-label, randomised, non-inferiority trial. Lancet 2026; published online July 7. doi:10.1016/S0140-6736(26)00851-2
Martucci G, Giani M, Schmidt M, et al. Anticoagulation and bleeding during veno-venous extracorporeal membrane oxygenation: insights from the PROTECMO study. Am J Respir Crit Care Med 2024; 209: 417–26
McMichael ABV, Ryerson LM, Ratano D, et al. 2021 ELSO adult and pediatric anticoagulation guidelines. ASAIO J 2022; 68: 303–10
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

A thirty-four-year-old for a hernia repair. After induction the pressure falls to fifty systolic, and the trainee reaches for adrenaline. The echo shows a thick septum, a tiny cavity and the mitral leaflet slapping into the outflow tract — and the pressure gets much worse.
This episode is the cardiomyopathies: the main types, how they present, what they look like on echo, and why getting the label right changes what you do with your hands.
We start with a definition and a simple way to hold the big three in your head — the ventricle that can't squeeze, the one that squeezes too well and won't relax, and the one that can't fill. Then each in turn. Dilated cardiomyopathy: the causes the exam wants, functional mitral regurgitation, apical thrombus, and the anaesthetic plan for a patient with a failing, afterload-sensitive ventricle, including devices and SGLT2 inhibitors. Hypertrophic cardiomyopathy: diagnosis, systolic anterior motion and the dagger-shaped outflow signal, why the anaesthetic goals run opposite to almost everything else we do, and what mavacamten means for theatre. Restrictive cardiomyopathy: amyloid, the low-voltage ECG with thick walls, and apical sparing on strain.
Then the mimic that matters — constrictive pericarditis versus restriction, why telling them apart is the difference between a curable and an incurable disease, the echo and cath lab discriminators, and the handbook's rules for a pericardiectomy. We finish with arrhythmogenic right ventricular cardiomyopathy and takotsubo, which can obstruct too.
The wrap-up is an echo spot-test: six pictures, six diagnoses — and six different treatments for the same low blood pressure.
Chapters
(00:00) Cold open — the wrong drug for a thick heart
(00:40) Definition and classification
(01:50) Dilated cardiomyopathy: causes, presentation and echo
(03:20) Ischaemic or non-ischaemic?
(03:40) Anaesthesia for dilated cardiomyopathy
(05:15) Hypertrophic cardiomyopathy: presentation and echo
(06:40) When is it obstructive?
(07:15) Anaesthetic goals in obstruction
(08:10) Long-term treatment, including mavacamten
(08:40) Restrictive cardiomyopathy and amyloid
(10:15) Strain imaging and apical sparing
(10:50) Constrictive pericarditis: the mimic
(11:30) Telling constriction from restriction
(12:50) Anaesthesia for pericardiectomy
(13:30) Arrhythmogenic right ventricular cardiomyopathy
(14:25) Takotsubo
(15:25) Echo spot-test
Key takeaways
A cardiomyopathy is disease of the heart muscle not explained by coronary, hypertensive, valvular or congenital disease
Dilated: can't squeeze — big round ventricle, functional MR, apical thrombus risk; avoid tachycardia and negative inotropy; it tolerates a modest fall in afterload
Turn off ICD shock therapies for diathermy, and stop SGLT2 inhibitors before surgery (euglycaemic ketoacidosis)
Hypertrophic: wall ≥15 mm (≥13 mm with family history); obstruction is a gradient ≥30 mmHg, significant at ≥50
In obstruction, fill them, slow them, use phenylephrine or vasopressin, and stop the inotropes — adrenaline can be fatal
Mavacamten lowers contractility and can push the ejection fraction down — know if your patient is on it
Restrictive: can't fill — big atria, normal ventricles, restrictive filling and a low e′; amyloid gives thick walls, a low-voltage ECG and apical sparing
Constriction is curable: septal bounce, respiratory variation in mitral inflow, preserved e′ (lateral lower than septal) and discordant ventricular pressures
Pericardiectomy: no PEEP, vasopressors running before induction, and be ready to open the chest early
ARVC: young athlete, VT with a left bundle pattern, T-wave inversion V1–V3 and epsilon waves; takotsubo can obstruct the outflow tract
Echo before the inotrope — the same hypotension has different treatments depending on the ventricle
References / further reading
Arbelo E et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J 2023; 44: 3503–626
Ommen SR et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy. Circulation 2024; 149: e1076–e1126
Garcia MJ. Constrictive pericarditis versus restrictive cardiomyopathy? J Am Coll Cardiol 2016; 67: 2061–76
Ghadri JR et al. International expert consensus document on takotsubo syndrome (part I). Eur Heart J 2018; 39: 2032–46
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

Day one after mitral valve surgery. The monitor says the cardiac index is a healthy three point two. The lactate is six, the feet are cold and the urine has stopped. One of those numbers is lying — and it isn't the lactate.
This episode is cardiac output monitoring, for the exam and for the bedside: how each device works, the physiology underneath, when we actually use them, and where each one misleads you.
We start with first principles: cardiac output as heart rate times stroke volume, the exam definitions of preload, afterload and contractility, and why a normal blood pressure can hide a failing pump. Then the Fick principle, what a central venous saturation can and can't tell you, and how to diagnose a low-output state by looking at the whole patient rather than one number.
Then the devices, one by one. The pulmonary artery catheter — Stewart–Hamilton thermodilution, the continuous thermal-filament version, floating one by the waveforms, complications, the evidence from ESCAPE and PAC-Man, and why it's still the only monitor that shows you the right heart and the pulmonary circulation directly. PiCCO and LiDCO, and their volumetric extras. Uncalibrated pulse contour monitors, and the arrhythmias, valve leaks, vasoplegia and balloon pumps that break them. Stroke volume and pulse pressure variation, and why an open chest and a failing right ventricle make them unreliable. The oesophageal Doppler — the four assumptions behind its number. Echo, which gives you not just the number but the reason. Bioimpedance, and why it never caught on. And what the console really tells you on ECMO, a BiVAD or an implanted LVAD.
We finish with a quick-fire quiz, so you can test yourself on the lot.
Chapters
(00:00) Cold open — one of these numbers is lying
(00:50) The physiology: stroke volume, pressure and flow
(01:50) The Fick principle and venous saturations
(02:55) Diagnosing low output at the bedside
(03:55) The pulmonary artery catheter and thermodilution
(05:55) Floating a PA catheter by the waveforms
(07:25) Complications and the evidence
(09:05) Transpulmonary thermodilution — PiCCO
(10:20) Lithium dilution — LiDCO
(10:55) Uncalibrated pulse contour monitors
(12:00) Stroke volume and pulse pressure variation
(12:55) The oesophageal Doppler and its assumptions
(15:30) Echo: the number and the reason
(16:20) Bioimpedance and bioreactance
(16:55) Flow on ECMO, BiVADs and LVADs
(17:35) Putting it together
(18:05) Quick-fire quiz
Key takeaways
Cardiac output = heart rate × stroke volume; mean arterial pressure = cardiac output × SVR — so a normal pressure says nothing about which one is holding it up
Central venous saturation is not truly mixed venous, and it can mislead in both directions — low for reasons other than output, and high when the tissues can't extract oxygen
Diagnose low output from the whole patient: symptoms, signs, end-organ function, lactate and acidosis
The PA catheter is the reference standard (Stewart–Hamilton thermodilution); continuous versions use a thermal filament and lag behind sudden change
Know the waveforms — RA 0–8, RV 15–30/0–8, PA 15–30/4–12, wedge ~12 mmHg; never leave the balloon wedged; beware existing left bundle branch block
ESCAPE and PAC-Man showed no routine survival benefit — use it where the numbers will change what you do
PiCCO adds global end-diastolic volume and extravascular lung water, but needs regular recalibration; any thermodilution is unreliable on ECMO
Uncalibrated pulse contour is good for trends, poor in AF, aortic regurgitation, vasoplegia, a damped line or a balloon pump
SVV/PPV above ~12–13% predicts fluid responsiveness only in a fully ventilated, closed-chest patient in sinus rhythm
Oesophageal Doppler assumes a nomogram aortic area, a fixed 70:30 split, the right vessel at a sensible angle, and laminar flow; normal FTc 330–360 ms
Echo stroke volume = LVOT area × VTI — the diameter is squared, so small errors grow; its real value is telling you why the output is low
On ECMO or a BiVAD the console shows circuit flow only; an LVAD estimates flow from power and speed
References / further reading
Binanay C et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005; 294: 1625–33
Harvey S et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005; 366: 472–7
Marik PE et al. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med 2009; 37: 2642–7
Cecconi M et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014; 40: 1795–815
Teboul JL et al. Less invasive hemodynamic monitoring in critically ill patients. Intensive Care Med 2016; 42: 1350–9
Follow the podcastBluesky: @cardiacoutput.bsky.socialX: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice.

Forty minutes into an aortic valve replacement, the cross-clamp is on and the heart is arrested. Then a little electrical activity starts creeping back on the ECG. What do you do? Tell the surgeon — out loud, straight away — because that heart is waking up while it's still ischaemic. The anaesthetist is part of myocardial protection, even though the solution runs through the perfusionist's pump.
This episode is cardioplegia from the top end of the table. We start with why it exists: the moment the aorta is clamped, the heart has no coronary flow, and a warm, beating, ischaemic heart runs out of energy in minutes. Cardioplegia makes planned ischaemia survivable in five ways — arrest, cool, empty, feed and buffer, and limit reperfusion injury — and arrest does most of the work.
Then what's in the bag, grouped the way examiners like it: an arresting agent, buffers, osmotic agents and substrate. How potassium produces a depolarised arrest by inactivating fast sodium channels, and why that isn't quite a resting membrane. Why the commonest solution is 4:1 blood cardioplegia, and what blood adds over crystalloid. Warm versus cold as a real trade-off — and the hot shot that gets the heart ready before the clamp comes off.
Delivery routes next. Antegrade into the aortic root as standard, direct into the ostia, or down the vein grafts. Retrograde through the coronary sinus for aortic regurgitation, aortic and root surgery, and severe coronary disease — with the 40 mmHg limit on coronary sinus pressure, why retrograde protects the right ventricle less well, and how to confirm the cannula on TOE. And why antegrade into a regurgitant root distends the ventricle instead of perfusing it.
Then the seven complications — trauma, air, oedema, bleeding, difficulty restarting, electrolyte disturbance and inadequate protection — and how the last one really shows up: as a heart that comes off badly. del Nido, with its single long-acting dose, lidocaine and low calcium. Custodiol (HTK), which arrests the heart by taking the sodium away rather than adding potassium, and the price you pay in volume and dilution. And Laplace's law, which explains why a distended ventricle is dangerous and why we vent — during surgery, with a balloon pump, and on VA-ECMO.
We finish with the anaesthetist's checklist during the cross-clamp, and what to be ready for when it comes off.
Chapters
(00:00) Cold open — the ECG wakes up during the cross-clamp
(01:00) Why we need cardioplegia, and the five mechanisms
(01:50) How much oxygen arrest and cooling save
(02:30) What's in the bag
(02:40) Potassium and the depolarised arrest
(04:10) Buffers, osmotic agents and substrate
(04:50) Blood versus crystalloid
(05:40) Warm versus cold
(06:30) The hot shot
(07:00) Antegrade delivery
(07:40) Retrograde delivery, and when you need it
(08:00) Why antegrade fails with aortic regurgitation
(08:40) The coronary sinus pressure limit, and the right ventricle
(09:20) Confirming the retrograde cannula on TOE
(10:00) The seven complications
(12:20) del Nido
(13:30) Custodiol (HTK)
(15:00) Laplace's law, and why we vent
(16:00) The anaesthetist's checklist during the cross-clamp
(16:30) Wrap-up
Key takeaways
If electrical activity returns on the ECG during the cross-clamp, tell the surgeon straight away — the heart is working while ischaemic
Cardioplegia protects the heart in five ways: arrest, cool, empty, deliver substrate and buffering, and limit reperfusion injury — arrest does the heavy lifting
Contents fall into four groups: an arresting agent (usually potassium, with magnesium), buffers, osmotic agents and substrate
High potassium raises the resting membrane potential and inactivates fast sodium channels — a depolarised arrest in diastole
Blood cardioplegia (4:1) adds oxygen carriage, buffering, free-radical scavenging and better microvascular flow, with less oedema
Cold maximises metabolic suppression; warm supports aerobic metabolism; a warm "hot shot" before clamp removal prepares the heart for reperfusion
Retrograde delivery via the coronary sinus is used for significant aortic regurgitation, aortic valve and root surgery, and severe coronary disease — keep sinus pressure below 40 mmHg
Retrograde protects the right ventricle less well, so it's often combined with antegrade
In aortic regurgitation, antegrade root delivery distends the left ventricle — watch the LV on TOE and say if it's getting bigger
Complications: trauma, air, myocardial oedema, bleeding, difficulty restarting, systemic electrolyte disturbance and inadequate protection
del Nido (1 part blood to 4 crystalloid, with lidocaine and low calcium) gives a single dose lasting up to around 90 minutes
Custodiol (HTK) arrests by sodium depletion — a hyperpolarised arrest — with long protection, but large volumes cause haemodilution and hyponatraemia
Laplace: wall tension rises with pressure and radius — which is why distension is dangerous and why we vent
Solutions, doses and protocols are Wythenshawe-specific — check your own unit's practice
References / further reading
Gravlee GP et al., eds. Cardiopulmonary Bypass and Mechanical Support: Principles and Practice, 4th edn. Philadelphia: Wolters Kluwer, 2016
Matte GS, del Nido PJ. History and use of del Nido cardioplegia solution at Boston Children's Hospital. J Extra Corpor Technol 2012; 44: 98–103
Edelman JJB et al. Custodiol for myocardial protection and preservation: a systematic review. Ann Cardiothorac Surg 2013; 2: 717–28
Mackay JH, Arrowsmith JE et al., eds. Core Topics in Cardiac Anaesthesia, 3rd edn. Cambridge: Cambridge University Press, 2020 — myocardial protection chapter
Follow the podcast
Bluesky: @cardiacoutput.bsky.social
X: @CardiacOutputMC
If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered.
This podcast is for medical education for healthcare professionals. It is not clinical advice. Solutions, doses and practice described reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.