Cardiac Output

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.

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 trust the nasopharyngeal temperature — wait for a bladder temperature of 36.5–37°C
On echo, the surgeon needs to know why the valve leaks, not how badly
A dilated root, a stripped commissure or a prolapsing flap all mean the valve is repairable
Intrinsically diseased cusps or a destroyed annulus mean replacement — and an unstable patient may need the quicker operation
Octaplex for DOAC reversal: we know it works, and it's at the bedside
Washing jets are normal; if they're coagulopathic, leave the chest open
References / further reading
Isselbacher EM et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation2022
Erbel R et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J 2014
Boodhwani M et al. Repair-oriented classification of aortic insufficiency. J Thorac Cardiovasc Surg 2009
Schäfers HJ et al. Cusp geometry and effective height in aortic valve repair. J Thorac Cardiovasc Surg 2006
Hahn RT et al. Guidelines for performing a comprehensive transoesophageal echocardiographic examination. J Am Soc Echocardiogr 2013
Davies EA, Charlesworth M, Agarwal S. Hypertensive emergencies. BJA Education 2024
Boer C et al. EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. 2017
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.

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 rather than boluses to avoid overshoot
Alpha blockade before beta in phaeochromocytoma — beta blockade alone is contraindicated
PRES is a clinical and radiological diagnosis, and can occur in normotensive patients
References / further reading
Davies EA, Charlesworth M, Agarwal S. Hypertensive emergencies. BJA Education 2024
Isselbacher EM et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation2022
Erbel R et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J 2014
van den Born BJ et al. ESC Council on Hypertension position document on the management of hypertensive emergencies. Eur Heart J Cardiovasc Pharmacother 2019
Williams B et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J 2018
Connor D, Boumphrey S. Perioperative care of phaeochromocytoma. BJA Education 2016
Fischer M, Schmutzhard E. Posterior reversible encephalopathy syndrome. J Neurol 2017
This podcast is for medical education for healthcare professionals. It is not clinical advice. Drugs and doses discussed reflect local practice or quoted international guidance at the time of recording — always follow your own centre's guidelines and current local policy.

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 softer criteria than a general ICU — because overload and acidosis tip the RV over
Low-dose adrenaline on VA-ECMO keeps the heart ejecting so the pulmonary circulation doesn't go stagnant
Pace a transplanted heart at 110: stroke volume is fixed, so output is all rate
Make the VA-ECMO decision before the patient spirals, not during
References / further reading
Velleca A et al. ISHLT Guidelines for the Care of Heart Transplant Recipients. J Heart Lung Transplant 2023
Snell GI et al. ISHLT Working Group report on primary graft dysfunction: definition and grading. J Heart Lung Transplant 2017
Hoetzenecker K et al. Extracorporeal support in lung transplantation: intraoperative and postoperative strategies. J Thorac Cardiovasc Surg 2020
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)
Mathew R et al. DOREMI: milrinone vs dobutamine in cardiogenic shock. NEJM 2021
NHS England. Adult Extracorporeal Membrane Oxygenation Service Specification
This podcast is for medical education for healthcare professionals. It is not clinical advice. All drugs and doses discussed reflect local Wythenshawe protocol at the time of recording — always follow your own centre's guidelines and current local policy.

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 bypass for lung transplant: less anticoagulation, less bleeding, and the heart keeps beating
Protect the new lung — room air, 3–4 mL/kg, under 20 cmH₂O — because hyperoxia drives primary graft dysfunction
Coming off, follow the ladder: inotropes → pacing → IABP → nitric → VA-ECMO, and don't re-heparinise
Be certain it's vasoplegia before giving methylene blue; in a low output state it is a brick wall in front of the heart
Put the vascath in yourself in theatre rather than leaving it to the unit
References / further reading
Velleca A et al. ISHLT Guidelines for the Care of Heart Transplant Recipients. J Heart Lung Transplant 2023
Leard LE et al. ISHLT consensus document for the selection of lung transplant candidates. J Heart Lung Transplant2021
Snell GI et al. ISHLT Working Group report on primary graft dysfunction: definition and grading. J Heart Lung Transplant 2017
Ius F et al. Lung transplantation on cardiopulmonary support: VA-ECMO versus cardiopulmonary bypass. J Thorac Cardiovasc Surg 2012
Diamond JM et al. Clinical risk factors for primary graft dysfunction after lung transplantation. Am J Respir Crit Care Med 2013
Levin RL et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg 2004
Boer C et al. EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. 2017
This podcast is for medical education for healthcare professionals. It is not clinical advice. All drugs and doses discussed reflect local Wythenshawe protocol at the time of recording — always follow your own centre's guidelines and current local policy.

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 after cardiovascular procedures: pathophysiology and targeted therapy. J Cardiothorac Vasc Anesth 2018
Mathew R et al. DOREMI: milrinone vs dobutamine in cardiogenic shock. NEJM 2021
Mehta RH et al. LEVO-CTS: levosimendan in patients with reduced EF undergoing cardiac surgery. NEJM 2017
Ibrahim M et al. Modern management of systolic anterior motion of the mitral valve. Eur J Cardiothorac Surg 2012
Boer C et al. EACTS/EACTA Guidelines on patient blood management for adult cardiac surgery. 2017
This podcast is for medical education for healthcare professionals. It is not clinical advice — always follow your local protocols and your own centre's guidance.

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 education for healthcare professionals. It is not clinical advice — always follow your local protocols and your regional cardiac / ECMO centre's guidance.

It's three in the morning. Your patient is proned, paralysed, on 100% oxygen, and his P/F ratio is 70. Do you keep cranking the ventilator — or do you pick up the phone?
In this episode Mike and Calum work through veno-venous ECMO the way it actually gets used on an ICU: what it does, who it's for, and the things that catch people out at the bedside.
We cover the single most important idea in ECMO — that it doesn't treat anything, it's a bridge — and why that reframes every decision you make. We get into the physiology consultants love to quiz you on (sweep gas for CO2, blood flow for oxygen, and why a septic, hyperdynamic patient can desaturate with a perfectly functioning circuit). We walk through who actually qualifies, using the EOLIA and CESAR thresholds, the Murray score, and the harder question of whether the lungs have a plausible route back.
Then we take an honest look at the evidence. CESAR randomised to referral, not to ECMO. EOLIA was stopped for futility with an 11% mortality gap — and we unpick why the 28% crossover in the control arm makes "negative trial" the wrong conclusion, and what the individual-patient-data meta-analysis and the COVID-era NHS England data added.
Finally, the practical half: the nationally commissioned UK centres (now including Barts, Bristol and Newcastle) and how to make a referral that gets your patient assessed fast; cannulation configurations; lung-rest ventilation and the bleeding-versus-clotting balancing act; and a rapid-fire troubleshooting round — recirculation, the suddenly desaturating patient, line chatter, and the failing oxygenator. Plus why Harlequin syndrome is a VA problem, not a VV one.
Chapters
(00:00) Cold open — 3am, and a P/F of 70
(01:16) What ECMO actually is (and isn't)
(03:22) Sweep vs flow — the physiology you'll be quizzed on
(05:22) Who actually gets cannulated: EOLIA, CESAR, Murray, RESP
(07:02) Optimise first — and prone them
(07:40) The evidence, honestly: CESAR and EOLIA
(10:15) The UK service: 8 commissioned centres
(11:11) Cannulation and configurations
(12:31) Day-to-day: lung rest and anticoagulation
(13:54) Troubleshooting at 2am
(16:07) Harlequin — why it's a VA problem
(16:49) Weaning and the sweep-off trial
(17:49) Wrap-up
Key takeaways
ECMO is a bridge, not a treatment — no bridgeable destination, no bridge
Sweep gas controls CO2; blood flow controls oxygenation
VV-ECMO provides no haemodynamic support — preserved cardiac function is a prerequisite
Optimise and prone before you refer
Recirculation is the VV gremlin; Harlequin is a VA phenomenon
References
Peek GJ et al. CESAR trial. Lancet 2009
Combes A et al. EOLIA trial. NEJM 2018
Goligher EC et al. Bayesian re-analysis of EOLIA. JAMA 2018
Combes A et al. CESAR/EOLIA individual patient data meta-analysis
ELSO Guidelines: Management of Adult Patients Supported with VV-ECMO (2021)
NHS England Adult ECMO Service Specification
Camporota L et al. Outcomes of the NHS England National ECMO Service. BJA 2021
This podcast is for medical education for healthcare professionals. It is not clinical advice — always follow your local protocols and your regional ECMO centre's guidance.