Cardiac Output

Episodi

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  TOE for Mechanical Support 2: VADs and the Impella 13.09.2026 24min

  People say ”VAD” and mean five different machines. Which ventricle, how long, surgical or percutaneous — then the septum tells you the rest.
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  TOE for Mechanical Support 1: Balloon Pumps and ECMO 13.09.2026 16min

  In mechanical circulatory support, TOE isn’t an investigation you order — it’s part of the device. Balloon pump positioning, cannulas and recirculation.
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  Cardiopulmonary Bypass: What It Does to the Patient 12.09.2026 23min

  Naming the parts of a bypass circuit is the easy half. The marks are in what each component does to the person on the table.
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  Intra-Aortic Balloon Pumps: Timing, Traces and Trials 11.09.2026 27min

  The balloon pump has had a bad decade in the literature, and a lot of people have drawn the wrong conclusion from it. Physiology, traces, timing and the trap.
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  Journal Club: Iron Before Cardiac Surgery (ITACS) 07.09.2026 20min

  A new BMJ trial says intravenous iron buys an extra day at home. We read the methods — including the primary outcome that was changed mid-trial.
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  Protamine: The Most Dangerous Drug We Give Every Day 05.09.2026 18min

  There’s a reason the consultant gives the protamine themselves. Plus heparin rebound, aprotinin’s effect on your TEG, and an emergency BiVAD in acute HIT.
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  Bleeding After Cardiac Surgery: Products, TEGs and HIT 04.09.2026 21min

  The drains are filling and your instinct is to send a TEG. Why that may be the wrong move — plus FFP versus Octaplex, cryo versus concentrate, and HIT properly.
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  Endocarditis Surgery: Timing, Bleeding and Vasoplegia 29.08.2026 19min

  More than half of endocarditis patients need surgery. When to operate, why the delay is the point, and the two escalations that will catch you out.
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  Endocarditis for Residents: Cultures, Criteria and Echo 28.08.2026 18min

  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-associa
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  What Would You Do? Cognitive Bias in ECMO Decisions 13.08.2026 16min

  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
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  Check the Tube. Then Check It Again. 12.08.2026 15min

  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
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  TAVI for Residents: Evidence, Rapid Pacing and Sedation 09.08.2026 21min

  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
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  Empty, Not Vasoplegic: Aortic Stenosis After Surgery 08.08.2026 19min

  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 overe
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  VV-ECMO for Residents: Candidacy, Runs and Oxygenators 07.08.2026 20min

  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 arou
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  You Can't Clamp a Torn Aorta: DHCA Explained 05.08.2026 21min

  Here's the puzzle. Your patient has an acute type A dissection, so the ascending aorta is torn. To do cardiac surgery you need to cannulate the aorta and cross-clamp it — but the ascending aorta is both dissected and the thing you're about to operate on. So you can't cannulate it, and you can't clamp it. What do you do? The answer is that you cool the patient right down and stop the circulation altogether. In this episode Mike and Calum work through major aortic surgery and deep hypothermic circulatory arrest — the theatre half of the topic. The ICU half, on hypertensive emergencies and acute aortic syndromes, is the previous episode. Please note: the drugs and doses discussed are Wythenshawe-specific local practice. Take the principles, and check your own guidelines for the numbers. We start with the arrest itself: why the anaesthetist stays in the room, cooling to 18°C with ice packed round the head, and thiopentone to drop the cerebral metabolic rate. Then cannulation — femoral or right axillary — and the trap that follows, because if they clamp the right axillary artery your arterial line and saturation probe need to be on the left. We cover selective antegrade cerebral perfusion, why cerebral oximetry is your window on the only organ you can't afford to lose, and what the anaesthetist, perfusionist and surgeon can each do about low cerebral saturations. Then rewarming, and a strong opinion: after circulatory arrest, the nasopharyngeal probe tells you a comfortable lie. Believe it and you'll come off bypass cold, and hand over a patient who then cools further, drops their cardiac output and becomes vasoplegic and coagulopathic. Wait for the bladder temperature. The centrepiece is an echo walkthrough of the aortic root, because it directly decides the operation. The four levels of the root, the two workhorse views, and the question that actually matters — not how badly the valve leaks, but why. We work through the three mechanisms of aortic regurgitation in dissection (a dilated root pulling normal cusps apart, a commissure stripped off the wall by the flap, and the flap itself prolapsing through), all of which mean the valve is a victim rather than the culprit and can potentially be saved. Then what forces replacement, why an unstable patient may be better served by a quicker operation, and how to scan the finished repair. We finish with DOAC reversal and why certainty at the bedside beats elegance in a paper, washing jets versus paravalvular leaks, postoperative goals, and where CSF drainage fits for descending aortic work. Chapters (00:00) Cold open — the aorta you can't clamp (01:30) Cooling to 18°C: how the arrest protects the brain (03:20) Cannulation, and why your art line goes on the left (05:00) Cerebral perfusion, oximetry and low saturations (06:40) Knowing the surgeon's plan — the essence of cardiac anaesthesia (07:40) The cross-clamp, and why there isn't one during arrest (08:40) Rewarming: the temperature probe that lies to you (10:30) Echo deep dive: the four levels of the aortic root (12:00) The views — and asking why it leaks, not how badly (13:30) Three mechanisms of AR: the valve as victim (15:00) When to replace, and why time changes the operation (16:30) What else to report: ostia, tamponade, entry tear (17:40) Scanning the finished repair (18:40) They've arrived on a DOAC (20:00) Washing jets versus paravalvular leaks (21:00) Postoperative goals and CSF drainage (22:00) Wrap-up Key takeaways You cannot cannulate or clamp an aorta that is both dissected and the operative site — hence circulatory arrest Cool to 18°C, ice the head, and give thiopentone: both cooling and barbiturate reduce cerebral oxygen demand If the return goes to the right axillary artery, put your arterial line and saturation probe on the left During the arrest itself there is no cross-clamp at all — nothing is flowing Cerebral oximetry is your window on the brain, and low saturations are a three-way conversation Do not
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  Think Aorta: Hypertensive Emergencies and Dissection 04.08.2026 18min

  A thirty-five-year-old with chest pain, a bit sweaty, a bit anxious, and a blood pressure that's frankly high. In a lot of departments that patient gets a troponin, a D-dimer, possibly a label of anxiety — and goes home. If that pain was an acute type A dissection, they are not going to get better. In this episode Mike and Calum work through hypertension and the acute aortic syndromes as they actually present — the intensive care half of the topic. The theatre half, on deep hypothermic circulatory arrest, is the next episode. Please note: the drugs and doses discussed are either local Wythenshawe practice or suggestions quoted from international guidance. Take the principles, and check your own guidelines and local policy for the numbers. We start with a distinction people use interchangeably and shouldn't: emergency versus urgency. It hangs entirely on hypertension-mediated organ damage — acute damage to the heart, retina, brain, kidneys or large arteries — and the counterintuitive consequence is that severe hypertension without organ damage does not mandate emergency treatment. Meanwhile HMOD can occur at normal blood pressure readings, because the rate of change matters more than any threshold. Then the disease itself. The syndromes that should raise your suspicion — Marfan, Turner, bicuspid aortic valve, Ehlers-Danlos — and the trap that these patients are usually not under surveillance, because nobody has ever diagnosed them. Stanford and DeBakey classification, roughly one percent mortality per hour for the first forty-eight hours, and the contrasting logic for a chronic aneurysm, where you watch and wait until 5.5 cm in the ascending aorta or 6.5 cm descending. We're fair about why it gets missed, and honest about the consequence: treat it as an ACS or a PE and you anticoagulate a patient who was going to bleed anyway. What they need is a CT chest and a phone call to a cardiac centre. Finally, the pharmacology done properly. Why heart rate matters as much as pressure — shear stress relates to dP/dt, so you're blunting the impulse, not just the number. Labetalol versus esmolol, the personalities and downsides of GTN, magnesium and hydralazine, and the two ways to hurt someone with treatment: overtreatment and overshoot, causing watershed infarction, mesenteric ischaemia and acute kidney injury. Plus the thing to do before any antihypertensive at all — treat the pain. We close with phaeochromocytoma (alpha blockade first, always) and PRES, the one that needs the scan as well as the clinical picture. Chapters (00:00) Cold open — the chest pain that gets sent home (01:20) Emergency vs urgency: it's the organ damage, not the number (03:30) The syndromes — and why nobody has diagnosed them (05:30) Stanford, DeBakey, and one percent an hour (07:20) The chronic aneurysm: watch, or operate? (09:00) Why type A dissections get missed (10:40) Preoperative goals and anti-impulse therapy (12:30) The drugs and their personalities (14:20) Overtreatment, overshoot — and treating pain first (15:50) Phaeochromocytoma: alpha before beta, always (17:00) PRES — the one that needs the scan (18:00) Wrap-up Key takeaways A hypertensive emergency is defined by acute hypertension-mediated organ damage, not by the number — and HMOD can occur at normal blood pressures Hypertensive urgency, without organ damage, does not mandate emergency treatment Patients presenting with dissection are often undiagnosed — it may be the first time anyone has looked at them properly Type A is any dissection involving the ascending aorta; roughly 1% mortality per hour for the first 48 hours Chronic aneurysm is different logic: surveillance, then operate above 5.5 cm ascending or 6.5 cm descending It gets missed as ACS, PE, acute abdomen or anxiety — and those patients arrive anticoagulated Treat pain first, then anti-impulse therapy: shear stress is about dP/dt, not just peak pressure Target systolic 100–120 and a rate of 60–70, using an infusion rathe
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  Heart and Lung Transplants: The First 48 Hours in ICU 02.08.2026 24min

  The operation is over. The new heart and lungs are in, and the patient has just arrived on the unit. This is where you actually earn your keep. In this episode Mike and Calum work through the first forty-eight hours after a heart or lung transplant — and almost everything comes back to one structure: the right ventricle. This is the postoperative ICU half; the theatre half is the previous episode. Please note: the drugs and doses discussed are Wythenshawe-specific local protocol, and are given as a worked example of how one centre does it. Take the principles, and check your own guidelines for the numbers. We start with why the RV dominates everything — because when these patients fail, it happens almost without you noticing, and by the time you've understood the trajectory you're reopening the chest. That drives how you ventilate them: keep intrathoracic pressures low, but hold normocarbia, because letting the CO₂ drift causes pulmonary vasoconstriction and starts the spiral. We call it the Goldilocks zone. Then the mechanical support decisions. Why a lung transplant with wet lungs or a long ischaemic time comes out on veno-arterial rather than veno-venous ECMO — a practical answer, not a physiological one — and the real cost of a long VA run, including patients returning for serial tracheal dilatations years later. We cover a piece of institutional learning worth hearing: heart transplants were once cannulated on the strength of a damped radial trace, when a femoral line would have shown straightforward vasoplegia that fluid and time would fix. Hence two arterial lines, always, and the radiofemoral difference. We also make the case for leaving the chest open when things haven't been straightforward, the deliberately soft threshold for filtration, and the counterintuitive reason you might run low-dose adrenaline on VA-ECMO — to keep the heart ejecting, so the bypassed pulmonary circulation doesn't go stagnant and clot. Finally: why a transplanted heart is paced at 110 (a fixed stroke volume makes cardiac output almost entirely rate-dependent), milrinone as a first choice with the honest admission that inotropes are an art rather than a science, immunosuppression and whether the patient is actually absorbing it, the BiVAD and VV-ECMO bridges and why we want those patients awake and off cardioactive drugs — and how to manage acute RV dysfunction before the spiral rather than during it. Chapters (00:00) Cold open — the hard bit isn't the operation (01:00) Why everything comes back to the right ventricle (02:30) Ventilating for the RV: the Goldilocks zone (05:00) Why lung transplants come out on VA rather than VV ECMO (07:00) The bronchial anastomosis cost of a long ECMO run (08:20) Heart transplants and the damped radial trace (10:30) Two arterial lines and the radiofemoral difference (12:00) Open or closed chest — being realistic with the surgeons (14:00) Renal replacement: much softer criteria than you'd expect (15:40) Adrenaline on VA-ECMO — keeping the heart ejecting (17:30) Pacing at 110 and the fixed stroke volume (19:30) Milrinone, and why inotropes are an art (21:00) Immunosuppression — and whether they're absorbing it (22:30) The BiVAD bridge: awake, rehabbed, off cardioactive drugs (24:00) VV-ECMO as a bridge to lung transplant (25:30) Acute RV dysfunction — deciding before the spiral (26:40) Wrap-up Key takeaways Everything after a heart or lung transplant comes back to the right ventricle — and RV failure arrives fast enough that you have to be ahead of it Ventilate for the RV: low intrathoracic pressures but normocarbia, normoxia and a normal pH Lung transplants come out on VA-ECMO because the cannulas are already there — but a long run risks the bronchial anastomosis Two arterial lines, always: the radiofemoral difference distinguishes vasoplegia from low output and can spare someone an unnecessary cannulation If it's been anything other than straightforward, leave the chest open Filter early — much
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  Heart and Lung Transplants: The Twelve Hours in Theatre 01.08.2026 27min

  The phone goes at eleven at night. There's a donor heart, and it's coming here. In a few hours that organ is going into a patient who is, right now, sitting on a ward waiting for you. In this episode Mike and Calum work through heart and lung transplantation from the listing call to the handover on the unit — the twelve hours in the middle. This is the theatre half; the postoperative ICU episode is separate. Please note: the drugs and doses discussed are Wythenshawe-specific local protocol, and are given as a worked example of how one centre does it. Take the principles, and check your own guidelines for the numbers. We start upstream of theatre — candidacy as a gift of life, why the patients being transplanted now are sicker and more borderline than a decade ago, and why compliance and mental health belong in that conversation. Then the middle-of-the-night listing assessment: what the reg is actually there to check, and what's already been done for you. Then into theatre. Preparation that has to happen before the patient arrives (products in the fridge, six units of red cells from the start, pacemaker to fixed mode, immunosuppression before they leave the ward). Induction drugs, including the vitamin K that stops the rebound phenomenon in a warfarinised LVAD explant. And a proper walk through the lines — why the femoral venous sheath is an escape route for a balloon pump wire, why the right-sided line is shorter to dodge the caval snare, and the Swan you must remember to withdraw before bicaval cannulation. For lungs we cover risk stratification up to "extreme high risk" — where you cannulate the groin before you induce, with a primed circuit and two consultants plus an ECMO consultant scrubbed — lung isolation, and the elegant argument for VA-ECMO over full bypass. Then the first implant: inflating to 15–20 cmH₂O, loosening the PA clamp, the three causes of hypotension at that moment, and the deliberately austere protective strategy for a new lung (FiO₂ 0.21, 3–4 mL/kg, under 20 cmH₂O) because hyperoxia drives primary graft dysfunction. Finally the sharp end: the written escalation ladder coming off bypass — milrinone, dopamine and noradrenaline, then sequential pacing, then the balloon pump, then nitric at 20 ppm, then conversion to VA-ECMO — and why you do not re-heparinise. Plus vasoplegia and its most dangerous trap: give methylene blue to a patient who is actually in a low cardiac output state and you have put a brick wall in front of the heart. We finish with the TOE numbers for the pulmonary vein and PA anastomoses, and an end-of-case checklist that includes putting the vascath in yourself. Chapters (00:00) Cold open — a donor heart is coming (01:00) Candidacy: who gets a transplant, and the MDT (03:20) The middle-of-the-night listing assessment (05:10) Preparation before the patient arrives (06:40) Induction drugs — and vitamin K for LVAD explants (08:20) Lines, and the traps that catch people out (11:00) The extreme high-risk lung induction (12:40) Lung isolation and positioning (13:40) Baseline TOE and metabolic management (14:40) Why transplants need so much insulin (15:40) Antifibrinolytics: tranexamic acid and aprotinin (16:30) Why VA-ECMO beats bypass for lungs (18:00) The first lung in: de-airing and protective ventilation (20:00) ECMO flow problems on the table (20:50) Coming off bypass: the escalation ladder (23:40) Vasoplegia — and the methylene blue brick wall (25:40) Low-volume blood products (26:40) TOE after implantation: the PV and PA numbers (28:00) End of case, vascaths and handover Key takeaways A transplant is a gift of life — candidacy is an MDT decision, not a 3am one Build your escape routes at the start: a femoral sheath that will take a balloon pump wire, a short right-sided line to clear the caval snare, and a Swan withdrawn before bicaval cannulation For the sickest lungs, cannulate the groin before you induce — with the room already full of the right people VA-ECMO beats bypa
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  Cardiac Theatre for Residents: Vasoplegia, SAM and Pacing 26.07.2026 16min

  Your noradrenaline is climbing, and climbing, and the pressure still won't hold. The tank's the right size and the pump is working — so what do you reach for next? In this episode Mike and Calum get scrubbed for the theatre half of the cardiac topic: the problems that show up on the table rather than on the unit, and the ones that catch people out. This is the companion to the ICU episode on heart failure and mechanical circulatory support. We start with vasoplegia — when to add vasopressin, why a femoral arterial line earns its place (the radiofemoral difference tracks the severity, and it takes days rather than hours to close), and the second-line agents: methylene blue at 1 mg/kg, why you warn the surgeon before you give it, and high-dose hydroxocobalamin when that isn't enough. Then a quick tour of the inotropes — and the honest admission that there is no perfect one, and essentially no evidence on which is best in acute heart failure. Then the moment everyone dreads: coming off bypass with a failing right ventricle. Get the rate up, get atrial wires in, nitric on, inotropes running — and choose Octaplex and fibrinogen over big volumes of FFP and cryo, because bleeding in the face of RV failure is one of the hardest balancing acts in the building. We cover SAM — systolic anterior motion — which is easy to miss, hard to manage, and can have you telling a surgeon there's a problem with a valve that's perfectly fine. Finally, a proper deep dive on pacing, from the epicardial wires up: why you nag for atrial wires, how to read the three-letter code, what AAI, DDD, VVI and the asynchronous modes actually do, and when diathermy forces your hand. We finish on the two dials everyone muddles — output and sensitivity — and the counterintuitive trap at the heart of it: turning the millivolt number up makes the box less sensitive, which is how you end up pacing onto a T wave. R-on-T is the commonest cause of cardiac arrest on a cardiac ICU, and NAP7 says so. Plus a closing bugbear about vascaths. Chapters (00:00) Cold open — the noradrenaline that won't hold (00:50) Vasoplegia: vasopressin, and the radiofemoral difference (02:20) Methylene blue and hydroxocobalamin (03:50) The inotropes — and why there's no perfect one (05:00) Cardiac output monitoring in theatre (06:00) Coming off bypass with a failing RV (07:40) SAM — systolic anterior motion (09:00) Pacing deep dive: the wires and the three-letter code (10:30) AAI, DDD, VVI — and the atrial kick (12:00) Asynchronous modes and diathermy (13:00) Output vs sensitivity — the trap that causes R-on-T (14:40) NAP7, and the daily bedside discipline (15:40) Permanent pacemakers: checks and mode agreement (16:20) The vascath bugbear (17:00) Wrap-up Key takeaways Escalate vasoplegia in order: noradrenaline → vasopressin → methylene blue → hydroxocobalamin A femoral arterial line earns its place — the radiofemoral difference tracks the degree of vasoplegia There is no perfect inotrope, and almost no evidence on which is best in acute heart failure A failing RV coming off bypass wants rate, atrial wires, nitric and inotropes — and low-volume factor concentrates rather than FFP and cryo SAM is dynamic LVOT obstruction — manage it by filling and pacing, not by blaming the valve Nag for atrial wires: no atrial wire means you're stuck in VVI Set output at 2–3× the capture threshold, and re-check daily as the wires fibrose Sensitivity is inverted — a higher millivolt setting makes the box less sensitive; undersensing causes R-on-T, the commonest cause of arrest on a cardiac ICU (NAP7) References / further reading Royal College of Anaesthetists. 7th National Audit Project (NAP7): perioperative cardiac arrest. 2023 Reade MC. Temporary epicardial pacing after cardiac surgery: a practical review. Anaesthesia 2007 (parts 1 and 2) Levin RL et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg 2004 Shaefi S et al. Vasoplegia aft
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  Mechanical Circulatory Support in ICU: Cardiac Output, VA-ECMO and VADs 24.07.2026 18min

  It's the middle of the night (again). Your post-op cardiac patient looks awful, and the nurse says the cardiac output's low. Do you reach for a number — or do you look at the patient? In this episode Mike and Calum work through heart failure and mechanical circulatory support the way it actually plays out on a cardiothoracic ICU: how you know the output is low, what the devices really do, and how to escalate before it's too late. This is the intensive care half of the topic — the theatre half is a separate episode. We start with the idea that cardiac output is a clinical diagnosis, not a single figure — why venous sats and the Fick principle are clues rather than answers, and the picture that actually tells you the pump is failing (the tachycardia they're leaning on, the deranged liver enzymes and kidneys, the rising lactate, and the low-output gut that gets mistaken for an acute abdomen). We cover the pulmonary artery catheter — still the gold standard against a field of derived monitors — and how to float one, trace by trace. Then the machines. We give you the single most important habit on the unit — on any patient on support, always work out where the cannulas are and where the blood is going — and use it to walk through VA-ECMO (and why bypassing the heart and lungs means stagnation, clot, and a patient you usually can't wake), BiVADs (both sides supported, awake for weeks), and the ambulatory LVAD (why its flow is derived from power, why it's preload-dependent and afterload-sensitive, and why the shocked HeartMate patient in Emergency Department needs fluid before you pick up the phone). Finally, the practical half: escalating heart failure up the ladder — milrinone, then dopamine, then the balloon pump, and by then you're knocking on the door of a mechanical support assessment — plus inhaled nitric, a monitoring trap with the axillary return line, an honest look at ECMO-CPR, and why Harlequin syndrome is the signature limitation of peripheral VA-ECMO. Chapters (00:00) Cold open — 3am, and "the cardiac output's low" (01:00) Low cardiac output: why it's not a single number (03:30) The pulmonary artery catheter — gold standard, and how to float one (06:30) The golden rule: always find the cannulas — and VA-ECMO (08:30) BiVADs: supporting both sides, awake for weeks (10:00) LVADs and the HeartMate 3: flow is derived, not measured (12:10) Escalating heart failure: milrinone, dopamine, the balloon pump (14:40) The axillary return line — a monitoring trap (15:30) ECMO-CPR: the evidence and the criteria (17:20) Harlequin — the VA payoff (18:10) Wrap-up Key takeaways Cardiac output is a clinical diagnosis, not a number — venous sats and monitors are clues, not answers On any support device, always work out where the cannulas are and where the blood is flowing VA-ECMO bypasses heart and lungs — it clots, it's temporary, and you usually can't wake the patient; the elegant fix is femoral drainage with an axillary return LVAD flow is derived from power — it's preload-dependent and afterload-sensitive, so when in doubt, give fluid Milrinone → dopamine → balloon pump is the escalation ladder; a balloon pump means an MCS assessment is close Harlequin (differential hypoxaemia) is the signature limitation of peripheral VA-ECMO References / further reading Binanay C et al. ESCAPE trial: pulmonary artery catheter in advanced heart failure. JAMA 2005 Mathew R et al. DOREMI: milrinone vs dobutamine in cardiogenic shock. NEJM 2021 Mehra MR et al. MOMENTUM 3: HeartMate 3 (fully magnetically levitated LVAD). NEJM 2019 Ostadal P et al. ECMO-CS: early VA-ECMO in cardiogenic shock. Circulation 2023 Stub D et al. CHEER trial: refractory arrest, ECMO and cooling. Resuscitation 2015 Suverein MM et al. INCEPTION: ECPR vs conventional CPR in refractory out-of-hospital arrest. NEJM 2023 McDonagh TA et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021 This podcast is for medical educ