Cardiac Output

Something different this episode. No 3am emergency — instead, a pre-assessment clinic on a Tuesday afternoon, a woman booked for an aortic valve replacement in six weeks, and a haemoglobin of 118. Do you give her intravenous iron?
ITACS, published in The BMJ in August 2026, is the best answer we have ever had to that question. It is also a trial with a great deal to teach about how to read a paper properly — so this is a journal club, and we go through the methods slowly, because that is where the meaning lives.
The question first. A third of patients coming for cardiac surgery are anaemic, twenty to fifty per cent are transfused, and both are powerfully associated with complications, longer stays and death — in a specialty that consumes around ten per cent of the entire NHS blood supply. Correcting the anaemia in clinic attacks both problems at once. But anaemia may be a marker as well as a mechanism: if patients do badly because of the kidney disease or inflammation that made them anaemic, then fixing the number fixes the screen and changes nothing about the patient. A strong prognostic marker is not automatically a treatment target — and that idea runs through the whole episode.
Then the methods. Thirty-three hospitals across ten countries, 955 anaemic adults for elective cardiac surgery, a single 1,000 mg dose of intravenous iron or placebo one to twenty-six weeks beforehand — and, deliberately, no requirement to prove iron deficiency. We look at how you blind a brown drug (a black syringe and an opaque line), and at the detail that separates a good trial from a trial that merely says "double blind" in its abstract: they checked whether the masking had worked by asking patients to guess their allocation.
The primary outcome is days alive and at home at 90 days — what it captures, and the two things it hides. And then the finding that isn't in the abstract at all: the primary outcome was originally days at home at thirty days, and was amended to ninety in December 2020. We give the defence and the concern, and then we look at what the original outcome showed. It was null. Had the investigators kept it, this would be a negative trial, and that belongs in any honest summary of the paper.
The results deserve care. The iron worked biochemically — ferritin rose from around 110 to over 500 — but haemoglobin rose by under 4 g/L, and three quarters of treated patients were still anaemic on the day of surgery, which explains the size of everything that follows. The primary result is one day, with a confidence interval touching zero, in a trial powered for a day and a half. Transfusion is the solid finding: 68% down to 61%, about fifteen patients treated to prevent one transfusion, and roughly 44 units of blood saved per hundred patients. But length of stay was identical, complications were identical — so where did the extra day come from? The paper answers it, and the answer is a smaller claim than the headline sounds.
The best thing in the trial isn't in the abstract either. Rather than only reporting the median, the investigators reported the treatment effect across the whole distribution — and it turns out that patients who recovered well gained a fraction of a day, while at the 25th centile the difference was 6.1 days. All the benefit sits with the patients who did badly. It is post hoc, it was requested at peer review, and one of its confidence intervals is enormous — but it is biologically coherent, and it may be the most important idea to come out of this trial.
We also correct an argument we would have made before reading the full paper. The obvious criticism — that enrolling patients without proven iron deficiency dilutes the effect — was pre-specified, tested, and not supported. Calum then supplies the more sophisticated objection, which is that an interaction test in a trial this size cannot exclude a subgroup difference. Plus the safety signal that matters to us specifically: a sixteen-fold increase in hypophosphataemia.
We finish with the four-point critique, the strengths the trial genuinely deserves, and what to do in clinic on Monday.
Chapters
(00:00) Cold open — a haemoglobin of 118 and six weeks to go
(01:00) Why the question matters, and the ten per cent of the blood supply
(02:10) Marker or mechanism? The idea that runs through everything
(03:00) What we knew before ITACS
(03:40) The methods: 33 hospitals, 955 patients, no iron deficiency required
(04:40) How do you blind a brown drug — and how do you prove it worked?
(05:40) Days alive and at home: what it captures and what it hides
(07:10) The primary outcome was changed mid-trial
(08:30) What the original outcome showed
(09:20) Sample size, two interim analyses, and the 95.4% interval
(10:30) Did the iron actually do anything? Under 4 g/L
(11:40) The primary result — one day, and an interval touching zero
(12:50) Transfusion: the solid finding
(13:50) Same length of stay, same complications — so where did the day come from?
(15:00) The result the headline misses: who actually benefited
(16:30) Iron deficiency — an argument corrected, and a better objection
(18:00) Safety, and the phosphate
(18:40) The critique in four parts
(19:30) The strengths, and Monday morning
(20:30) Wrap-up
Key takeaways
Anaemia is a marker as well as a mechanism — a strong prognostic marker is not automatically a treatment target
ITACS: 33 hospitals, 10 countries, 955 anaemic adults, a single 1,000 mg dose of IV iron or placebo, 1–26 weeks before elective cardiac surgery
The primary outcome was changed from days at home at 30 days to 90 days in December 2020 — and the original outcome was null
Always ask what a trial's original primary outcome was, and what it showed
The iron filled the stores but raised haemoglobin by under 4 g/L, and three quarters of treated patients were still anaemic on the day of surgery
Primary result: one extra day at home in 90, with a confidence interval touching zero, in a trial powered for 1.5 days
Transfusion is the robust finding: 68% to 61%, NNT about 15, and roughly 44 units of blood saved per 100 patients treated
Length of stay and complications were identical — the extra day accrued after discharge as shorter readmissions, not fewer of them
A post hoc quantile analysis suggests all the benefit sits with the poor recoverers: 6.1 days at the 25th centile against a fraction of a day at the 75th
Benefit was the same with or without demonstrable iron deficiency — but that interaction test is underpowered, so read it as no reason to restrict treatment rather than proof that deficiency is irrelevant
Intravenous iron caused a sixteen-fold increase in hypophosphataemia, which is not a footnote in a patient about to be weaned
The 95.4% confidence interval is the fingerprint of pre-planned interim analyses and alpha spending
Find the anaemia early: the biggest barrier in this trial was time, not biology
Read the methods before the abstract, and convert every relative number into an absolute one
References / further reading
Myles PS, Klein AA, Smith JA, et al. Intravenous iron to treat anaemia before cardiac surgery (ITACS): international, double blind, placebo controlled randomised trial. BMJ 2026; 394: e100407
Myles PS, Richards T, Klein A, et al. Rationale and design of the intravenous iron for treatment of anemia before cardiac surgery trial. Am Heart J 2021; 239: 64–72
Boer C et al. 2017 EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. J Cardiothorac Vasc Anesth 2018
Agarwal S, Choi SW, Fletcher SN, Klein AA, Gill R. The incidence and effect of resternotomy following cardiac surgery on morbidity and mortality: a 1-year national audit on behalf of the Association of Cardiothoracic Anaesthesia and Critical Care. Anaesthesia 2021; 76: 19–26
Myles PS et al. Validation of days at home as an outcome measure after surgery. BMJ Open 2017
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 paper you'd like taken apart.
This podcast is for medical education for healthcare professionals. It is not clinical advice. Discussion of published research reflects our own reading and interpretation — always read the primary source and follow your own centre's guidelines.

You will have noticed that consultants tend to give the protamine themselves, and if you're an ST3 who hasn't done much cardiac, nobody asks you to do it. Most people assume that's habit. It isn't.
This is the theatre half of the bleeding week — the drugs, the traps in the tests, and a salvage case at the far end of what's possible. Last episode was the unit.
Please note: the doses and drug choices are Wythenshawe-specific local practice. Take the principles, and check your own guidelines.
The scale first: cardiac surgery consumes around ten per cent of the entire NHS blood supply, and ninety per cent of those products go into ten per cent of patients. Which makes anticipating who that will be most of the job. Bypass is hostile to clotting in five ways at once — a large heparin dose, haemodilution, cooling, platelet activation and consumption, and contact with the circuit — so know the cases where you will predictably need products (deep hypothermic circulatory arrest, redos, long pump runs, transplants and VAD explants, endocarditis, and anyone arriving anticoagulated) and act on it while they're still on bypass. Order them, get them thawed, get them physically in the room. The worst position is realising you need four units of something that's still in a freezer twenty minutes away.
Then the antifibrinolytics. Tranexamic acid at three to four grams is the modern default; aprotinin — Trasylol — was withdrawn in 2008, reintroduced in 2012 with very narrow licensing, and is now used off-license for high bleeding risk, with the honest admission that there is very little evidence directly comparing the two. And a trap the crib sheet asks about directly: aprotinin artificially prolongs the R time on your TEG, so the trace suggests a coagulopathy that isn't there and you can go chasing it with products the patient doesn't need.
We do the acquired von Willebrand story properly, because it's lovely physiology: turbulent flow across a tight aortic valve shears platelets and cleaves the large von Willebrand multimers, so the valve lesion itself causes a bleeding disorder — and explains the patient who oozes at the end of an aortic valve replacement for no other obvious reason. DDAVP, twenty micrograms in a hundred millilitres, given slowly, because giving it fast to a marginal patient at the end of a case will drop their pressure.
The centrepiece is protamine. What it actually does (electrostatic neutralisation, not a receptor effect), the three types of reaction, and why type three — profound pulmonary vasoconstriction, pulmonary hypertension and right ventricular failure — is the one that empties the ventricle and stops the heart. Then the technique that follows from the principle that when you decide to stop, no more protamine must reach the patient: not through a running flush with a column of drug behind it, but through the central line with the tap turned between patient and syringe. And the counterintuitive part — protamine in excess is itself an anticoagulant, so the generous dose given "to be sure" makes the patient oozier, not drier.
Heparin rebound gets its own section, because it's the four-in-the-morning diagnosis that saves a patient a lot of unnecessary products: protein-bound and extravascular heparin redistributing into a circulation whose protamine has already been cleared. Unexplained oozing in a patient who left theatre dry needs a small further dose of protamine, not factors. We also cover heparin resistance as an antithrombin problem, and recombinant factor seven — including a real case where it arrived from another hospital by ambulance and stopped the bleeding immediately, with proper caveats about cost, availability, thrombosis and haematology authorisation.
We finish at the salvage end: a patient with acute HIT and thrombotic complications who needs an emergency BiVAD, with no time for plasma exchange or immunoglobulin. Heparin is out, argatroban is a unit drug rather than a theatre one, and almost nobody is comfortable with bivalirudin. The answer starts with getting the right surgeon — because some will go onto cardiopulmonary bypass first, and a bypass circuit demands full anticoagulation. Instead: VA-ECMO first as a heparin-free run, then the BiVAD from there, decided at a full MDT that is honest about what this is. And for the patient with HIT who needs surgery but isn't an emergency, the first and best intervention is simply time.
Chapters
(00:00) Cold open — the most dangerous drug we give
(00:50) The scale: ten per cent of the blood supply
(01:40) Why bypass is hostile to clotting
(02:30) Who predictably needs products — and acting while still on bypass
(03:40) Tranexamic acid, and aprotinin
(05:20) Aprotinin prolongs the R time — don't chase it
(06:10) Acquired von Willebrand disorder in aortic stenosis
(07:40) DDAVP, and why you give it slowly
(08:50) Protamine — what it does and why it's dangerous
(10:00) The three types of reaction
(11:00) Giving it so that stopping means stopping
(12:20) Too much protamine is an anticoagulant
(13:00) Heparin rebound — the 4am diagnosis
(14:40) Heparin resistance and antithrombin
(15:40) Recombinant factor seven, and the ambulance
(17:20) Acute HIT needing an emergency BiVAD
(19:40) After the salvage: no platelets, and buying time
(20:30) Elective HIT: delay is the treatment
(21:40) Bivalirudin, if you had to
(22:40) Wrap-up
Key takeaways
Cardiac surgery uses around 10% of the NHS blood supply, and 90% of those products go to 10% of patients — anticipate, and get products thawed and in the room while the patient is still on bypass
Bypass impairs clotting five ways: heparin, haemodilution, cooling, platelet activation and consumption, and circuit contact
Tranexamic acid 3–4 g is the default; aprotinin is off-license for redos and high bleeding risk, with little comparative evidence
Aprotinin prolongs the R time on the TEG — don't chase a coagulopathy that isn't there
Severe aortic stenosis causes acquired von Willebrand disorder through shear; DDAVP 20 micrograms in 100 mL, given slowly, and cryoprecipitate is a rational choice
Protamine neutralises heparin by charge, and can cause pulmonary hypertension, RV failure and cardiac arrest
Type 1 is rate-related hypotension, type 2 anaphylactoid, type 3 the catastrophic pulmonary vasoconstriction — type 3 is what kills
Give protamine so that stopping means stopping: no flush behind it, tap turned between patient and syringe
Excess protamine is itself an anticoagulant — titrate it, don't pour it in
Unexplained oozing hours later on the unit is heparin rebound: give more protamine, not more products
Heparin resistance is an antithrombin problem — antithrombin III around 500 units, not more heparin
Recombinant factor seven works but is expensive, hard to locate, prothrombotic and needs haematology sign-off
For emergency surgery in acute HIT: the right surgeon, VA-ECMO before the BiVAD, a heparin-free run, no platelets, and an MDT honest about it being salvage
Where there is time, time is the treatment — delay towards remote HIT, plasma exchange, IVIG, and a single intra-operative heparin exposure only
References / further reading
Boer C et al. 2017 EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. J Cardiothorac Vasc Anesth 2018
Task Force et al. 2024 EACTS/EACTAIC Guidelines on patient blood management in adult cardiac surgery
Myles PS et al. Tranexamic acid in patients undergoing coronary-artery surgery (ATACAS). N Engl J Med 2017
Fergusson DA et al. A comparison of aprotinin and lysine analogues in high-risk cardiac surgery (BART). N Engl J Med 2008
Nybo M, Madsen JS. Serious anaphylactic reactions due to protamine sulfate: a systematic literature review. Basic Clin Pharmacol Toxicol 2008
Vincentelli A et al. Acquired von Willebrand syndrome in aortic stenosis. N Engl J Med 2003
Cuker A et al. American Society of Hematology 2018 guidelines: heparin-induced thrombocytopenia. Blood Adv2018
Koster A et al. Anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia. Ann Thorac Surg
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. All drugs and doses discussed reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines.

Two in the morning, day zero after cardiac surgery. The chest drains have been filling steadily for an hour, the nurse is looking at you, and the surgical registrar is on the phone. Your instinct is to send a TEG and wait for it to tell you what to do — and that instinct, the one we are all taught, may be exactly what harms this patient.
This is the intensive care half of the bleeding week: resternotomy, blood products, point-of-care testing and heparin-induced thrombocytopenia. Mike takes a deliberately unfashionable position on the TEG and defends it, and Calum pushes back.
Please note: the doses and product choices are Wythenshawe-specific local practice. Take the principles, and check your own guidelines and transfusion policy.
We start with the thing everyone is trying to avoid — going back. Resternotomy for bleeding happens perhaps a couple of times a week, and once a patient needs a second procedure the odds of a poor outcome climb sharply: more red cells, more acute kidney injury and filtration, prolonged intubation, tracheostomy and a longer intensive care stay. Some of that is confounding, since you don't get taken back unless something has already gone wrong, but the UK audit data is clear enough. Which makes prevention one of the real jobs of the cardiac anaesthetist: stop the dual antiplatelets a week or two beforehand, insist on a proper period of haemostasis at the end of the case, and don't let surgeons close wet chests. If the patient is oozing, the chest gets packed, you give products, you give it time, you get them warm — and if they still aren't dry, you encourage the surgeon to leave the chest open. That is a good decision, not a failure of the operation, and the conversation needs diplomacy.
Then the products, in the two pairs that get confused constantly. FFP is human plasma, so it contains everything — all the factors plus fibrinogen, albumin, protein C and S and antithrombin III — but it comes at high volume, and pushing four units in fast can cause real problems for the right ventricle. Octaplex is four-factor prothrombin complex — factors two, seven, nine and ten — made up at the bedside, low volume, titratable, with around three thousand units to reverse warfarin or a DOAC, and a thousand units often enough to dry up needle-hole oozing that isn't responding to protamine. Then cryoprecipitate versus fibrinogen concentrate, where the newer, more expensive product isn't automatically the better one: cryo also carries von Willebrand factor and factor XIII, and in a patient with the acquired von Willebrand disorder that severe aortic stenosis gives you, the "inferior" product may be exactly the right one.
The centrepiece is the argument about point-of-care testing. Algorithms beat individual judgement and point-of-care testing produces more restrictive transfusion than laboratory testing — but it hasn't yet shown better outcomes, and in a patient with very high drain output the danger is waiting for information before doing anything to stop the bleeding. In a genuinely bleeding cardiac patient the TEG is usually hard to interpret and normally tells you to give everything. Use it, but never let it delay treatment — and have a low threshold for a TOE, because tamponade is the diagnosis you cannot afford to miss while you're chasing numbers.
The second half is HIT, taken well past "platelets dropped, send a screen". A rare, immune-mediated, severe drug reaction with antibodies against the platelet factor four–heparin complex, causing platelet activation, thrombin generation and life-threatening thrombosis — a clotting disease with a low platelet count, and around six per cent mortality per day untreated. We cover the 4T score and why pre-test probability still matters when you're sending a test anyway, how to separate it from the far more common heparin-associated thrombocytopenia, the biphasic platelet pattern that should make you sit up after cardiac surgery, and why a count above 150 doesn't exclude it. Then the in-house immunoassay that rules out versus the functional assay that confirms, the acute and subacute categories, why platelet transfusion is contraindicated, and what plasma exchange and IVIG buy you. We finish with argatroban — a direct thrombin inhibitor that needs no cofactor — and a case where a patient was bridged straight onto warfarin instead, and thrombosed.
Chapters
(00:00) Cold open — the drains are filling, and your instinct may harm this patient
(01:10) Resternotomy, and what it costs the patient
(02:40) Preventing it: antiplatelets, haemostasis, and the wet chest
(04:20) Leaving the chest open, and how that conversation goes
(05:20) FFP versus Octaplex
(07:30) Doses, and a thousand units for oozing
(08:50) Cryoprecipitate versus fibrinogen concentrate
(10:40) More of an art than a science
(11:40) The unfashionable view on TEGs
(13:40) Don't miss the tamponade
(14:20) When does the patient go back?
(15:40) HIT — what it actually is
(17:00) The 4T score, and why pre-test probability matters
(18:20) The biphasic pattern, and what else confounds it
(20:00) In-house screen versus the functional assay
(21:40) Why platelets are contraindicated
(22:40) Plasma exchange and IVIG
(23:40) Argatroban — and the warfarin bridge that went wrong
(25:20) Wrap-up
Key takeaways
Going back to theatre for bleeding is a serious marker of poor outcome — more transfusion, more AKI, longer ventilation and longer stay
Prevention starts in theatre: stop dual antiplatelets, take a proper haemostatic pause, and never let a surgeon close a wet chest
If they still aren't dry, leaving the chest open is a good decision rather than a failure
FFP contains everything but at high volume — pushing it in fast can be very bad for the right ventricle
Octaplex is four-factor PCC, made up at the bedside, low volume and titratable; around 3,000 units reverses warfarin or a DOAC
A thousand units of Octaplex often settles needle-hole oozing that protamine hasn't fixed
Cryoprecipitate isn't simply the inferior product — it carries von Willebrand factor and factor XIII, which may be exactly what an aortic stenosis patient needs
Use the TEG, but never wait for it in the acutely bleeding patient — give products, tell the surgeon, and go back if you can't stop it
Have a low threshold for TOE, specifically to exclude tamponade
HIT is a prothrombotic disease with a low platelet count, and roughly 6% mortality per day untreated
Use the 4T score for pre-test probability, look for the biphasic platelet pattern, and don't be reassured by a count above 150
The in-house immunoassay rules out; the functional assay confirms — and both can be falsely negative
Platelet transfusion in acute HIT is contraindicated; plasma exchange and IVIG are what buy you heparin
Stopping heparin is necessary but not sufficient — argatroban is a direct thrombin inhibitor needing no cofactor, and you must never bridge a HIT patient onto warfarin alone
References / further reading
Agarwal S, Choi SW, Fletcher SN, Klein AA, Gill R. The incidence and effect of resternotomy following cardiac surgery on morbidity and mortality: a 1-year national audit on behalf of the Association of Cardiothoracic Anaesthesia and Critical Care. Anaesthesia 2021; 76: 19–26
Boer C et al. 2017 EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. J Cardiothorac Vasc Anesth 2018
Task Force et al. 2024 EACTS/EACTAIC Guidelines on patient blood management in adult cardiac surgery
Wikkelsø A et al. Thromboelastography or thromboelastometry to monitor haemostatic treatment. Cochrane Database Syst Rev 2016
Greinacher A. Heparin-induced thrombocytopenia. N Engl J Med 2015
Cuker A et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia. Blood Adv 2018
Warkentin TE, Greinacher A. Management of heparin-induced thrombocytopenia. Curr Opin Hematol 2016
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. All drugs, doses and product choices discussed reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and transfusion policy.

Last episode we diagnosed endocarditis. This one operates — and it opens on the number that reframes the whole disease: more than half of patients with endocarditis will meet the criteria for cardiac surgery.
Half of them go through one of the biggest operations a human being can have, while septic, followed by a long intensive care stay and very often a tracheostomy. And the outcomes remain poor — prosthetic valve endocarditis carries around a 27% one-year mortality, with device-related disease closer to a one in four risk of not getting home at all. As Mike puts it, we don't really tell people that when we consent them for a heart valve.
Please note: the drugs and doses discussed are Wythenshawe-specific local practice. Take the principles, and check your own guidelines.
We start with the endocarditis team — a couple of mornings a week, regional cases discussed, antibiotics and imaging reviewed, and surgery arranged when indicated. If you're the registrar in a district general hospital with a patient you think has endocarditis, there is a route in: ring your cardiac centre and ask for the endocarditis MDT. Don't sit on them.
Then the indications for surgery — prosthetic material, severe regurgitation, uncontrolled infection and embolic risk, with the vegetation sizes worth memorising — and the argument that matters most: timing. Guidance says emergency or urgent, and some read that as "theatre now". The case made here is that there is almost always a twenty-four hour window to bring that patient to intensive care first: filter them, take fluid off, start inotropes, fix the antibiotics, correct the metabolic mess. Because if you take a grossly overloaded septic patient, put them on bypass and repair their valve, they will not come off bypass. That day isn't a delay. It's what makes the operation survivable.
In theatre, the thing you must not forget: send tissue for 16S PCR. For a patient whose blood was sterilised by antibiotics before anyone took proper cultures, the valve in the surgeon's hand may be the only remaining chance to name the organism — and it decides their treatment for the next six weeks.
We cover repair versus replacement (aortic valves tend to be replaced; up to 80% of mitral valves can be repaired), and then two traps. First, these patients are thrombotic rather than coagulopathic — until they bleed, when it can be catastrophic. Second, heparin resistance: many arrive on a heparin infusion having depleted their antithrombin, so the answer is antithrombin III, not more heparin. Treat the cofactor, not the drug.
Then cytokine absorbers — what they are, why an endocarditis patient in particular gets one, and an honest account of the evidence, which is essentially "it probably won't harm and the rationale is strong". Vasoplegia gets the full stepwise ladder, with the warning that matters: be certain it isn't a low cardiac output state before you give methylene blue. We finish with post-operative ECMO, and a patient the team had agreed wasn't for mechanical support — until the decision was reversed on the table, and they went home.
Chapters
(00:00) Cold open — more than half need surgery
(01:20) The outcomes nobody mentions at consent
(02:30) The endocarditis team, and how to get a patient discussed
(04:00) Indications for surgery, and the vegetation sizes
(05:40) When not to operate
(06:40) The timing argument, from both sides
(08:40) Why the twenty-four hours makes the operation survivable
(10:00) Send the tissue: 16S PCR
(11:20) Repair or replace?
(12:30) Thrombotic, not coagulopathic
(13:40) Heparin resistance — treat the cofactor
(15:00) Cytokine absorbers, and honest evidence
(16:30) Vasoplegia, and the methylene blue warning
(18:00) Post-operative ECMO, and a decision reversed
(19:30) Prophylaxis for non-cardiac surgery
(20:40) Wrap-up
Key takeaways
More than half of patients with endocarditis meet the criteria for surgery, and the outcomes remain poor
Every suspected case should be discussed with an endocarditis team — there is a route in from any hospital
Operate for prosthetic material, severe regurgitation, uncontrolled infection or embolic risk; vegetations over 10 mm after an embolus, or over 15 mm in isolation
Surgery is contraindicated with intracranial haemorrhage or coma, but the restrictions around stroke have relaxed
There is almost always a twenty-four hour window to optimise — filter, inotropes, antibiotics, fluid off — and that isn't a delay, it's what lets them come off bypass
Send tissue for 16S PCR: it may be the only chance to identify the organism
Aortic valves tend to be replaced; up to 80% of mitral valves can be repaired
These patients are thrombotic rather than coagulopathic — but when they bleed it can be catastrophic
Heparin resistance is an antithrombin problem: give antithrombin III, not more heparin
Cytokine absorbers are used on rationale rather than randomised evidence — and they adsorb drugs too
Two arterial lines, and climb the vasoplegia ladder — but be certain it isn't low cardiac output before giving methylene blue
Needing ECMO after endocarditis surgery is a poor prognostic sign — but stay humble, because patients surprise us
References / further reading
Charlesworth M, Williams BG, Ray S. Infective endocarditis. BJA Education 2023
Delgado V et al. 2023 ESC Guidelines for the management of endocarditis. Eur Heart J 2023
Pettersson GB, Hussain ST. Current AATS guidelines on surgical treatment of infective endocarditis. Ann Cardiothorac Surg 2019
Kang DH et al. Early surgery versus conventional treatment for infective endocarditis. NEJM 2012
Boer C et al. EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. 2017
Levin RL et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg 2004
National Institute for Health and Care Excellence. Prophylaxis against infective endocarditis (CG64)
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. All drugs and doses discussed reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.

Cast your mind back to medical school. You were taught to examine a patient starting at the hands, looking for splinter haemorrhages, Osler's nodes and Janeway lesions. When did you last actually see any of them?
Not because we've stopped looking — because the disease has changed underneath us. In this episode Mike and Calum work through infective endocarditis: why it presents so differently now, how it gets diagnosed, and the traps that make it harder than it needs to be. This is the diagnosis and intensive care half; the theatre half is the companion episode.
Please note: antibiotic choices vary enormously between centres and even between regions. Everything here is illustrative — follow your own microbiology advice.
Endocarditis used to be a community disease, brewing over weeks, with time to develop immune-complex phenomena in the fingernails. It's now much more of an acute, hospital-associated disorder — roughly a third of cases are healthcare-associated, and those carry a higher mortality. And we generate the risk factors ourselves, with valves, pacemakers, indwelling catheters and dialysis lines.
We cover the organisms and how they differ by continent, HACEK (and why the lab needs warning about slow growers), and fungal endocarditis — rare, bulky and grim. Then the pathophysiology, which is more elegant than it first appears: a healthy valve is remarkably resistant to infection, so something has to damage it first. Turbulence injures the endothelium, a sterile vegetation forms from platelets and the clotting cascade, and that bland thrombus becomes the landing pad a later bacteraemia colonises. That two-hit sequence explains where vegetations sit and why any valve, device or structural disease makes a patient high risk.
Then the two pillars of the Duke criteria, both of which get routinely mishandled. Blood cultures are frequently done badly — one set, then Tazocin, and by the time the microbiologist rings the antibiotics are already in and everything comes back negative. You've manufactured your own culture-negative endocarditis. Echo access is the second problem, though a new generation of intensivists and anaesthetists confident with bedside scanning is changing the timeline. We give clean rules: transthoracic first, isolated right heart disease can stop there, but a prosthetic valve or any implantable device always needs a TOE.
The criteria themselves have grown up — surgical inspection of the valve is now a major criterion, and gated CT and nuclear imaging rescue the uncertain case. We're honest about the antibiotic evidence, which amounts to no high-quality randomised trials at all, and work through exactly why that trial is so hard to design. Then the specifics worth knowing: aminoglycosides are out for staphylococcal native valve disease, daptomycin and fosfomycin are in for MRSA, and rifampicin waits until the bacteraemia has cleared.
We finish with what gets mistaken for endocarditis on echo, built around a real diagnostic argument — a lesion that turned out to be a fibroelastoma, because it was on the wrong side of the valve, too smooth and too round, and the patient was far too well.
Chapters
(00:00) Cold open — what you were taught to look for at the hands
(01:10) Why the classical signs have vanished
(02:20) The organisms, and why they've changed
(03:40) HACEK, and warning the lab
(04:50) Fungal endocarditis
(05:50) The two-hit pathophysiology
(07:10) Risk factors: any valve, any device
(08:00) Blood cultures done badly
(09:20) Transthoracic, transoesophageal, and who must have one
(10:40) The criteria grow up: surgery, CT and nuclear imaging
(12:00) The antibiotic evidence — and how you'd design the trial
(13:30) Aminoglycosides, daptomycin and the rifampicin timing rule
(14:40) What gets mistaken for endocarditis on echo
(16:00) Wrap-up
Key takeaways
The disease has moved from the community into hospital — stop waiting for splinter haemorrhages
About a third of cases are healthcare-associated, and we create the risk factors with valves, devices and lines
HACEK organisms are slow-growing, so the lab needs warning or you'll get a falsely negative culture
Endocarditis rarely affects a normal valve: turbulence damages endothelium, a sterile vegetation forms, and bacteraemia colonises it
Vegetations sit on the upstream side of the valve, where the shear stress is
Take adequate blood for culture before the antibiotics, or you invent your own culture-negative case
Transthoracic first; isolated right heart disease can stop there; a prosthetic valve or device always needs a TOE
Surgical inspection of the valve is now a major criterion, and gated CT and nuclear imaging rescue uncertain cases
There is no high-quality randomised evidence behind the antibiotic regimens — and there are good reasons why
Aminoglycosides are out for staphylococcal native valve disease; daptomycin and fosfomycin are in for MRSA; rifampicin waits until the bacteraemia clears
Not everything shaggy is endocarditis — check the side, the shape, and the patient
References / further reading
Charlesworth M, Williams BG, Ray S. Infective endocarditis. BJA Education 2023
Delgado V et al. 2023 ESC Guidelines for the management of endocarditis. Eur Heart J 2023
Fowler VG et al. The 2023 Duke–ISCVID criteria for infective endocarditis. Clin Infect Dis 2023
Habib G et al. Recommendations for the practice of echocardiography in infective endocarditis. Eur J Echocardiogr
Cahill TJ, Prendergast BD. Infective endocarditis. Lancet 2016
National Institute for Health and Care Excellence. Prophylaxis against infective endocarditis (CG64)
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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. Antibiotic regimens and practice described are illustrative and vary by centre — always follow your own microbiology advice, local guidelines and current policy.

Important note: every case in this episode is completely fictitious. The scenarios are teaching constructs, invented to illustrate patterns of clinical reasoning. No case describes a real patient, and any resemblance to any individual is entirely coincidental.
In ECMO, the hard part is almost never the cannulation. Putting cannulas in and troubleshooting hypoxia are learnable. What's hard is the decision — and there's no textbook for it.
In this episode Mike and Calum work through four invented scenarios. In each one, Mike takes Calum to the point where a decision has to be made, asks what he'd do, and then reveals what happened. Every scenario has more than one entirely defensible answer, and in every one a cognitive bias is quietly doing the deciding.
We start with a young man who needs ECMO for trauma-related lung injury — and also has a traumatic brain injury. The reflex is that you can't anticoagulate intracranial contusions, but that reflex rests on an assumption modern circuits no longer require, and it crowds out one of the best prognostic groups we ever see. That's base rate neglect.
Then a patient at day forty, where a phrase appears in the notes almost daily: "he's been on for forty days." The number has become the argument. Duration isn't a diagnosis — and asking a different question ("what specifically is stopping him weaning?") turns up something entirely fixable. That's anchoring, with availability bias underneath it.
The third scenario is the subtlest, because nobody does anything wrong. A young woman is treated for severe pneumonia, correctly. Then she starts bleeding, and it's blamed on the anticoagulation — also a completely satisfying explanation. Two plausible answers in a row, each of which stops anyone completing the diagnosis. That's search satisficing, and it ends with a thirty-second rule you can use tomorrow.
The last scenario ends badly, deliberately. A single word in a CT report — "fibrosis" — carries a certainty the imaging doesn't support. A time-limited trial of steroids is agreed, with a review date set in advance. It doesn't work, and the patient dies. And the decision was still reasonable. Judging it by the result would be outcome bias — which leads to the most uncomfortable idea in the episode: when you decline, you almost never find out you were wrong, so the only errors you can see are the ones where you acted.
We finish with the full list — availability, conjunction, overconfidence, representativeness, diagnostic momentum, commission bias, the IKEA effect — and the one to end on, the GI Joe fallacy: the tendency to think that knowing about cognitive bias is enough to overcome it. It isn't. So we close with four things that genuinely help, none of which are clever.
Chapters
(00:00) Cold open — the hard part isn't the cannula
(00:50) Why these cases are fictional, and why the reasoning still isn't
(01:40) The referee problem: making calls you can't verify
(02:20) Case one: trauma lung injury, and a head injury
(04:50) Base rate neglect
(05:30) Case two: "he's been on for forty days"
(07:40) Anchoring to a number rather than a trajectory
(08:30) Case three: the bleeding everyone blames on the circuit
(11:00) Search satisficing — and a thirty-second rule
(11:50) Case four: one word in a CT report
(13:40) Outcome bias, and the asymmetry of declining
(14:40) The full list of biases
(15:30) The GI Joe fallacy, and what actually helps
(16:10) Wrap-up
Key takeaways
The hard part of ECMO is the decision, not the cannula — and there's no textbook for it
Base rate neglect: one alarming feature can crowd out a favourable underlying picture
A contraindication that feels absolute may be a modifiable risk — ECMO does not obligatorily mean full anticoagulation
Duration is not a diagnosis; ask what specifically is preventing weaning
A satisfying diagnosis stops the search — and two satisfying explanations in a row are worse
In a bleeding ECMO patient, ask whether it's the circuit bleeding or the disease bleeding. Dip the urine
A single word in a report can carry more certainty than the evidence behind it
A reasonable decision can produce a bad outcome; don't judge the decision by the result
When you decline, you rarely learn you were wrong — which should make everyone humbler about saying no
Time-limited trials turn an impossible decision into a manageable one
Knowing about cognitive bias does not protect you from it
References / further reading
Croskerry P. From mindless to mindful practice — cognitive bias and clinical decision making. NEJM 2013
Croskerry P. The importance of cognitive errors in diagnosis and strategies to minimise them. Acad Med 2003
Saposnik G et al. Cognitive biases associated with medical decisions: a systematic review. BMC Med Inform Decis Mak 2016
Baron J, Hershey JC. Outcome bias in decision evaluation. J Pers Soc Psychol 1988
Chang DW et al. Evaluation of time-limited trials among critically ill patients. JAMA Intern Med 2021
Kahneman D. Thinking, Fast and Slow. 2011
Extracorporeal Life Support Organization (ELSO) General Guidelines for Adult ECMO
This podcast is for medical education for healthcare professionals. It is not clinical advice. All cases are entirely fictitious and were created for teaching purposes only; they do not describe real patients. Always follow your own centre's guidelines and current local policy.

Something a bit different this episode. We've spent this series on pumps and valves and circuits — today it's the airway, and the lung you're deliberately collapsing.
Mike and Calum work through thoracic and cardiac airway management: one-lung ventilation, the difficult double-lumen tube, the shared airway, and a couple of scenarios that will catch you out badly if you haven't thought about them first.
Please note: this reflects local Wythenshawe practice, and a fair amount of personal preference — flagged as such where it isn't gospel. Check your own guidelines.
We start with how one-lung ventilation used to be taught — volume control, 500 mL, rate of 16, and it'll all be fine — and how completely that has changed. Bronchoscope before you turn them and again afterwards, because that tube will move. Then rather than picking numbers, find where the dependent lung actually sits on its compliance curve: start with low PEEP, hold the driving pressure constant, ramp the PEEP up a couple of centimetres at a time, and watch compliance. Most patients land around a PEEP of 6–8 with a driving pressure of 14–16 — and above 16 you're risking ventilator-associated lung injury. Driving pressure is the number to watch, not tidal volume.
Then hypoxia on one lung, where the textbook answer and the real answer differ slightly. Check the tube. Then check it again — are you actually on one lung and not down one lobe, and in the correct lumen? Most of the time that's the answer. Optimise the dependent lung before you touch the other side.
For the difficult double-lumen tube we cover a lubricated bougie inside the bronchial lumen with video laryngoscopy (a personal preference, and not uncontroversial), awake intubation for a truly predicted difficult airway, and exchanging a single-lumen tube over an airway exchange catheter — plus the answer that isn't a technique at all, which is asking for a second pair of hands early. Then rigid bronchoscopy and tracheal stenting: TIVA, rocuronium and sugammadex, depth of anaesthesia monitoring, and a Sanders jet ventilator on a genuinely shared airway.
The centrepiece is a scenario that can trick anyone: high airway pressures coming off bypass. The answer you must hold in mind is anaphylaxis — and every classic sign works against you. It may be something the perfusionist gave, a surgical dye, a cleaning solution or a coated line. The patient is completely covered, so you won't see a rash. They're hypotensive, but hypotension coming off bypass is expected anyway. And if you then try to extubate after a lot of fluid, you may find oedematous cords. Look at the patient, look for a rash, consider anaphylaxis, and give adrenaline.
We finish with anaesthetising a patient already on VV-ECMO (and why you must not do a tracheostomy on someone who isn't properly anaesthetised), restrictive pericarditis, the cardiac difficult airway, and ERAS — designing the whole anaesthetic backwards from the patient walking out.
Chapters
(00:00) Cold open — the lung you're deliberately collapsing
(00:50) How one-lung ventilation used to be taught
(02:00) Bronchoscope before and after you turn them
(02:50) Titrating PEEP against compliance
(04:20) When they don't tolerate one lung
(05:10) Hypoxia on one-lung ventilation — check the tube first
(06:30) The difficult double-lumen tube
(08:00) Rigid bronchoscopy and jet ventilation
(09:40) High airway pressures off bypass — think anaphylaxis
(11:30) Anaesthetising a patient already on ECMO
(12:40) Restrictive pericarditis and the cardiac difficult airway
(13:50) ERAS: designing the anaesthetic backwards
(15:00) Wrap-up
Key takeaways
One-lung ventilation has moved on: bronchoscope before and after turning them, because the tube moves
Titrate PEEP against compliance rather than picking numbers — usually 6–8, with a driving pressure of 14–16
Driving pressure is the number to watch; above 16 you're risking lung injury
If they desaturate on one lung, check the tube first — that's usually the answer
Optimise the dependent lung before doing anything to the non-dependent one
For a difficult double-lumen tube: bougie and video laryngoscopy, awake intubation, or exchange over a catheter — and ask for help early
Rigid bronchoscopy needs neuromuscular blockade; airway trauma is reported without it
High airway pressures off bypass should make you think anaphylaxis, because every classic sign is hidden or explained away
A patient on ECMO having a tracheostomy needs full anaesthesia and depth of anaesthesia monitoring
Turn the PEEP off in restrictive pericarditis, and have vasopressors ready at induction
In the cardiac difficult airway, protect the stomach for the TOE probe and bail out to awake intubation early
References / further reading
Lohser J, Slinger P. Lung injury after one-lung ventilation. Anesth Analg 2015
Amato MBP et al. Driving pressure and survival in the acute respiratory distress syndrome. NEJM 2015
Campos JH. Lung isolation techniques for patients with difficult airway. Curr Opin Anaesthesiol 2010
Ahmad I et al. Difficult Airway Society 2025 guidelines for management of unanticipated difficult intubation in adults. Br J Anaesth 2025
Royal College of Anaesthetists. 6th National Audit Project (NAP6): perioperative anaphylaxis. 2018
Levy JH, Adkinson NF. Anaphylaxis during cardiac surgery. Anesth Analg 2008
Engelman DT et al. Guidelines for perioperative care in cardiac surgery: ERAS Society recommendations. JAMA Surg 2019

Everybody asks how you anaesthetise a patient for a TAVI. The answer takes about four seconds: it's lidocaine into the groin. For more than 95% of our patients that is very nearly it — transfemoral, local anaesthetic, a little procedural sedation from a nurse, and they never meet an anaesthetist at all.
Which raises the obvious question: why do a whole episode on it? Because the fact that the anaesthetic is trivial does not make this a low-risk procedure — and our value here has almost nothing to do with giving an anaesthetic. That's the thesis of the episode.
Please note: the drugs and doses discussed are Wythenshawe-specific local practice. Take the principles, and check your own guidelines.
We start with scale. TAVI is arguably the biggest disruptor in medical practice of the last twenty years — from perhaps forty cases in the UK in the early years to several thousand annually now. While anaesthesia debated video laryngoscopy and TIVA, the cardiologists took a brand new procedure and generated randomised trial after randomised trial.
Then diagnosis done properly. How you derive the aortic valve area on TOE using the continuity equation — and why three separate measurements plus a geometric assumption, with the LVOT diameter squared, is a lot of places to be wrong. Hence the velocity ratio, the dimensionless index that cancels the LVOT area entirely and doesn't need the ventricle to generate a big gradient. Plus why gated CT with a calcium score now answers anatomy, feasibility, access and sizing in a single scan.
We cover who gets TAVI over surgery — and the point that surprises people, which is that almost anybody can have a surgical AVR, while TAVI is the fussy one, ruled out by access and anatomy. Then the evidence arc from PARTNER through NOTION, SURTAVI, PARTNER 3 and Evolut Low Risk, a defence of non-inferiority as exactly the right question here, and two honest problems: the patients we actually treat would never have met the trial inclusion criteria, and the trials are funded by the people selling the valves. Plus the warning signal for younger patients, where surgical explant of a TAVI valve carries a high mortality.
Finally the practical half: minimalist TAVI and the fall in mortality from over 5% to under 2%; why rapid ventricular pacing at over 200 for a few seconds is needed and how to avoid it altogether with a self-expanding valve; the complications, including a roughly one-in-five permanent pacemaker rate; what the published reports into a struggling centre actually identify (selection, expertise and governance — never the anaesthetic technique); conversion planning and a patient who dissected in the cath lab and did well anyway; the anaesthetic and sedation techniques when they are needed; the principles for the severe aortic stenosis patient, ending on patience; and the rest of the cath lab, including MitraClip.
Chapters
(00:00) Cold open — "it's lidocaine into the groin"
(01:10) Why a trivial anaesthetic doesn't mean a low-risk procedure
(02:10) TAVI as the biggest disruption in twenty years
(03:40) Grading the valve: the continuity equation and its errors
(05:30) Why the velocity ratio is the better number
(06:40) The gated CT that answers everything at once
(07:40) Who gets TAVI — and why TAVI is the fussy option
(09:10) PARTNER to Evolut: the evidence arc
(11:00) Two problems: external validity, and who funds the trials
(12:40) The warning signal for younger patients
(13:50) Minimalist TAVI, and the fall in mortality
(15:20) Rapid ventricular pacing — and when to avoid it
(16:40) Complications, and the one-in-five pacemaker
(17:50) When it goes wrong: selection, expertise, governance
(18:40) Conversion planning, and a patient who surprised us
(19:40) Anaesthesia, sedation, and the principle of patience
(20:40) MitraClip and the rest of the cath lab
(21:20) Wrap-up
Key takeaways
For over 95% of patients TAVI is local anaesthetic and light sedation — and that does not make it low risk
The continuity equation needs three measurements and a geometric assumption; the velocity ratio needs neither
Gated CT with a calcium score answers grading, anatomy, feasibility and access in one scan
Almost anyone can have a surgical AVR; TAVI is the fussy option, ruled out by access and anatomy
Non-inferiority is the right question, because the recovery benefits are so large
The evidence is excellent but generated in patients unlike ours — and funded by the valve manufacturers
Surgical explant of a TAVI valve carries a high mortality, which matters for younger patients
Minimalist TAVI has taken mortality from over 5% to under 2%, with fewer steps and less stroke
Rapid pacing stops the ventricle fighting the balloon; if they won't tolerate it, use a self-expanding valve
Roughly one in five need a permanent pacemaker — a genuine complication, though the rate is falling
Plan the conversion before you start: pericardial window, bypass, or neither
For the aortic stenosis patient: minimise demand, optimise supply — and above all, be patient
References / further reading
Charlesworth M et al. Anaesthesia support for transcatheter heart valve interventions: a narrative review. Anaesthesia 2025
Leon MB et al. PARTNER: TAVI in patients who cannot undergo surgery. NEJM 2010
Thyregod HGH et al. NOTION: TAVI versus surgery in lower-risk patients. J Am Coll Cardiol 2015
Reardon MJ et al. SURTAVI: TAVI versus surgery in intermediate-risk patients. NEJM 2017
Mack MJ et al. PARTNER 3: TAVI with a balloon-expandable valve in low-risk patients. NEJM 2019
Popma JJ et al. Evolut Low Risk: TAVI with a self-expanding valve in low-risk patients. NEJM 2019
Fukuhara S et al. Surgical explantation of transcatheter aortic bioprostheses. J Thorac Cardiovasc Surg 2021
Vahanian A et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2021
This podcast is for medical education for healthcare professionals. It is not clinical advice. All drugs and doses discussed reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.

It's two in the morning. Your patient had an aortic valve replacement this afternoon — good ventricle, off bypass without a fuss — and the noradrenaline has crept up again. Your general intensive care instinct says work out why they're vasoplegic and turn the pressors up. In this specific patient, that instinct is wrong. Nine times out of ten they aren't vasoplegic. They're empty.
In this episode Mike and Calum work through aortic stenosis and the problems it creates on the cardiac unit. This is the intensive care half; the cath lab half, on TAVI and sedation, is the next episode.
Please note: the fluids and practice described are Wythenshawe-specific. Take the principles, and check your own guidelines.
We start with why that patient is empty. Aortic stenosis is mechanically an outflow tract obstruction, so the ventricle hypertrophies against it — and this afternoon the surgeon fixed the obstruction, but the ventricle didn't get the memo. A thick, stiff, non-compliant ventricle is exquisitely preload-dependent, and reaching for the vasopressor instead of the fluid will have you chasing that patient all night. Expect to give five litres in twenty-four hours, expect them to be overloaded a few days later, and don't reach for albumin on day zero — because by the time it arrives, your patient is another litre behind.
Then the disease itself. Why symptoms are the prognostic trigger — a one-year mortality of fifty percent from the moment they appear — and the murky world of low-gradient aortic stenosis, where the gradient depends on a ventricle that can still generate it. The sickest patients are precisely the ones the measurement fails on, underestimating severity and overestimating valve area. We cover the velocity ratio, which is dimensionless and sidesteps the problem, the four classes of severe aortic stenosis, dobutamine stress echo for pseudo-severe disease, and why gated CT with a calcium score has displaced echo as the most important scan for structural heart disease.
We also cover the heart team and why anaesthetists and intensivists belong on it (we're generalists, and we're good at assessing risk — where once we were simply the brake at the end of the process), the causes of aortic stenosis, and what a right heart catheter actually tells you.
Finally, two things that land on the reg overnight. Out-of-hospital cardiac arrest — where the principles are the same wherever the patient is, and the cardinal rule is not to prognosticate early, because the picture genuinely changes and the story matters as much as the tests. And pacing: AAI is fine after grafts but dangerous after valve surgery, VVI backup at 30–40 is your safety net, interrogate the box daily, restore community settings before discharge — and if a patient arrests, look at the pacing box before you open the chest.
Chapters
(00:00) Cold open — the pressors that keep climbing
(01:20) Why the post-AVR ventricle is empty, not vasoplegic
(03:10) Five litres in twenty-four hours
(04:40) Why not albumin on day zero
(06:00) AS pathophysiology, and why symptoms change everything
(07:40) Low-gradient AS: when the gradient lies
(09:20) The velocity ratio and the calcium score
(11:00) The heart team, and why we're on it
(12:40) Causes of AS, and the right heart catheter
(14:00) Out-of-hospital arrest: don't prognosticate early
(16:00) Pacing: AAI after grafts, VVI backup after valves
(18:00) When TAVI patients come to ICU
(19:10) Wrap-up
Key takeaways
The post-AVR patient with a hypertrophied ventricle is preload-dependent — when the pressure sags they're usually empty, not vasoplegic
Five litres in 24 hours is normal here; expect overload and diuretics a few days later
Don't use albumin on day-zero hearts — it arrives too late to help, and there's no evidence one fluid beats another
Symptoms are the trigger in aortic stenosis: one-year mortality of 50% from the moment they appear
In low-gradient disease the gradient lies — it underestimates severity and overestimates valve area
The velocity ratio is dimensionless, so it sidesteps the geometric assumptions and the need for a high gradient
Gated CT with a calcium score has displaced echo as the key scan in structural heart disease
Anaesthetists and intensivists belong on the heart team because we're generalists and we assess risk
Never prognosticate early after an out-of-hospital arrest — go multimodal, and weigh the story alongside the tests
AAI is fine after grafts but dangerous after valve surgery; VVI backup at 30–40 is the safety net
If a patient arrests on the unit, look at the pacing box first
References / further reading
Vahanian A et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2021
Otto CM et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation 2021
Pibarot P, Dumesnil JG. Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction. J Am Coll Cardiol 2012
Clavel MA et al. Aortic valve calcification by computed tomography in aortic stenosis. J Am Coll Cardiol 2013
Nolan JP et al. European Resuscitation Council and ESICM guidelines 2021: post-resuscitation care. Intensive Care Med 2021
Dankiewicz J et al. TTM2: hypothermia versus normothermia after cardiac arrest. NEJM 2021
Royal College of Anaesthetists. 7th National Audit Project (NAP7): perioperative cardiac arrest. 2023
Charlesworth M et al. Anaesthesia support for transcatheter heart valve interventions: a narrative review. Anaesthesia 2025
This podcast is for medical education for healthcare professionals. It is not clinical advice. Fluids, drugs and practice described reflect local Wythenshawe protocol at the time of recording — always follow your own centre's guidelines and current local policy.

Our first episode covered veno-venous ECMO the way it gets examined: sweep for CO₂, flow for oxygen, who qualifies, and how to read CESAR and EOLIA honestly. This episode is everything we didn't say — not the physiology, but the service. How ECMO got here, who actually says yes to a referral, and the things that genuinely shorten a run.
Please note: this reflects local Wythenshawe practice. Take the principles, and check your own guidelines.
We start with the history, because it explains the present. The first patient was a road traffic accident victim in 1960s America — go and look at the photograph of the machinery. Then years in which ECMO was essentially associated with death, and genuine doubt that it solved anything. Then, around 2008 to 2010, everything arrived at once: swine flu, a patient in Scotland who had to be transferred to Sweden because we couldn't offer ECMO here, the political question that followed, CESAR out of Leicester, and observational data from Australia and New Zealand — who were ahead of us because their lung transplant organs travelled further and arrived with longer ischaemic times. NICE looked at all of it, concluded equipoise had been lost, and Wythenshawe won one of the bids.
Then candidacy, which is far less formulaic than it used to be. It's now an MDT decision with two, three or more consultants, and the ideal patient doesn't really exist anymore. We work through two contrasting referrals that show why: a patient with a BMI of 50–60 and acute asthma may be an easier yes than an older patient with a bad pneumonia — because reversibility and expected run length matter more than any single exclusion criterion.
We cover what COVID changed (bifemoral cannulation, awake patients, less sedation, better steroid timing), the actual rest settings for a newly cannulated patient, and the three levers that shorten runs: early tracheostomy, negative diuresis and sedation weaning — with the caveat that each is harmful at the wrong moment. Plus an honest answer to why tracheostomy on ECMO stays a consultant procedure.
Then the part that changes practice most: a failing oxygenator doesn't just impair gas exchange, it causes coagulopathy. A D-dimer in the tens of thousands, a fibrinogen refractory to daily transfusion, unexplained platelet drops with negative HIT screens. It looks like DIC and isn't — and the treatment is changing a membrane that may be oxygenating perfectly well. We finish with hypoxia troubleshooting (including the classic mistake of turning up the sweep gas), decannulation and the microbiology plan, and exactly how you lay out an ECMO patient to get them through a CT scanner.
Chapters
(00:00) Cold open — everything episode one didn't say
(00:50) A road accident in the 1960s, and the years ECMO meant death
(02:40) Swine flu, a patient sent to Sweden, and the political case
(04:10) CESAR, Australia, and why NICE decided equipoise was lost
(05:40) Why there won't be more UK trials
(06:40) Who gets ECMO now: the MDT, and two contrasting patients
(09:00) What COVID changed: bifemoral, awake, steroids
(10:30) Rest settings for a newly cannulated patient
(11:50) The three levers that shorten a run
(13:10) Why tracheostomy stays a consultant procedure
(14:20) The failing oxygenator that isn't failing
(16:00) Hypoxia on ECMO — and the sweep gas mistake
(17:30) Decannulation and the microbiology plan
(18:20) Taking an ECMO patient to CT
(19:10) Wrap-up
Key takeaways
ECMO went from a therapy associated with death to a commissioned national service because swine flu, a patient sent abroad and CESAR all arrived together
Equipoise has been lost in the UK, so don't expect further randomised trials here
Candidacy is an MDT decision — a very obese asthmatic may be an easier yes than an older patient with pneumonia, because reversibility and run length outrank single exclusions
Since COVID: bifemoral cannulation, awake patients, less sedation, better steroid timing
Ventilate gently — peak around 20, PEEP around 10, FiO₂ 0.5, rate 12 — because not thrashing the lung is where the benefit lives
Early tracheostomy, negative diuresis and sedation weaning shorten runs, but each is harmful at the wrong time
A failing oxygenator causes coagulopathy, not just poor gas exchange — change it even if gas exchange looks fine
For hypoxia: check cannula position, match ECMO flow to cardiac output, consider sedation — and don't turn up the sweep
Accept saturations around 92%; chasing a normal number leads to harm
Plan decannulation with microbiology, and recognise the post-decannulation SIRS response for what it is
References / further reading
Peek GJ et al. CESAR trial. Lancet 2009
Australia and New Zealand ECMO Influenza Investigators. ECMO for 2009 influenza A(H1N1) ARDS. JAMA2009
National Institute for Health and Care Excellence. Extracorporeal membrane oxygenation for severe acute respiratory failure in adults (IPG391), 2011
Combes A et al. EOLIA trial. NEJM 2018
Goligher EC et al. Bayesian re-analysis of EOLIA. JAMA 2018
ELSO Guidelines: Management of Adult Patients Supported with VV-ECMO, 2021
Camporota L et al. Outcomes of the NHS England National ECMO Service. BJA 2021
NHS England Adult Respiratory ECMO Service Specification
This podcast is for medical education for healthcare professionals. It is not clinical advice. Practice described reflects local Wythenshawe protocol at the time of recording — always follow your own centre's guidance and your regional ECMO centre.