Cardiac Output

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 slowing, squeezing, removing inotropy and 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.