Cardiac Output

Dr Mike Charlesworth
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Cardiac Output is a podcast on cardiothoracic anaesthesia and intensive care medicine. Dr Mike Charlesworth and Dr Calum Downes bring you tacit knowledge from a national transplant and ECMO centre — the reasoning that never makes it into the textbook.

  1. 4d ago

    Cheap Knowledge, Scarce Experience: Training Generation Alpha

    If you're listening to this in the car or at the gym, you're part of the argument in this episode. Mike talks through his new editorial in Anaesthesia, "Cheap knowledge, scarce experience: training Generation Alpha" — and Calum points out the irony of discussing it on a podcast, along with the paper's own warning that a poorly produced podcast can be less useful than a dry lecture. We cover how each generation of anaesthetists has handled knowledge, and why generative artificial intelligence changes not just access to knowledge but what written work can prove. Then assessment: why chatbots nearly passing the FRCA doesn't make the exam redundant, why the conditions of an exam matter more than its content, the changes coming to the FRCA from July 2027, and the inversion that the exam residents complain about most is now among the best-defended evidence we hold. Then the workplace — supervised learning events, entrustment, and the tacit, pattern-based skills that make an anaesthetist safe — and why the real crisis is not one of knowledge, but of how we recognise competence and experience. Plus the case for abolishing the written reflective entry, the trouble with generational stereotypes and learning styles, and what departments should do now. We finish by sorting training into cheap and scarce — and making the case for using podcasts for the cheap things, so the scarce things get the time. Chapters (00:00) Cold open — you're part of the argument (01:20) How each generation handled knowledge (02:35) Why Generation Alpha matters (03:30) What was scarce, generation by generation (04:30) What written work can now prove (05:25) Chatbots and the FRCA (06:40) The 2027 exam changes (07:45) The workplace and tacit knowledge (09:15) What needs to change (09:45) Abolish the written reflection (10:10) Generations, learning styles and the paradox (11:40) What should happen now (12:45) Declaring artificial intelligence use (13:10) Cheap or scarce? Key takeaways Generative AI changes not just access to knowledge but what written work can prove — the artefact no longer shows the thinking happened Generation Alpha (born 2010–2024) starts medical school from 2028 and may be the first cohort for whom AI is simply part of the learning environment AI text detectors are unreliable, which weakens the evidence from text-based portfolio entries even for the honest majority A chatbot's exam score says nothing about the inference drawn from a human candidate under closed-book, invigilated, timed conditions Open-book assessment tests a different construct — searching and appraising — not a worse one; the error is changing conditions without deciding what to measure From July 2027, the FRCA primary becomes two 80-question applied knowledge papers and the final written a single 100-question paper, without constructed responses The exam is now among the best-defended evidence of competence; much of the portfolio relies on trust Workplace-based assessment and entrustment by a named consultant can't be generated by AI — but need trained assessors and protected time The crisis is not one of knowledge but of recognising competence, experience and clinical exposure The written reflective entry was always a poor proxy; reflection happens in a person Generational differences confound age, period and cohort effects, and matching teaching to learning styles isn't supported Use efficient formats for information, reserve face-to-face time for scarce things — and don't confuse delivery preference with educational value References / further reading Charlesworth M. Cheap knowledge, scarce experience: training Generation Alpha. Anaesthesia 2026. doi:10.1111/anae.70452 Birkett L, Fowler T, Pullen S. Performance of ChatGPT on a primary FRCA multiple choice question bank. Br J Anaesth 2023; 131: e34–5 Cai SC, Tung AMS, Eslick AT. Performance of ChatGPT on a free-response anaesthesia primary examination. Br J Anaesth 2024; 133: 219–21 McLachlan J. Independent review of the assessment processes of the Royal College of Anaesthetists. 2023 Risko EF, Gilbert SJ. Cognitive offloading. Trends Cogn Sci 2016; 20: 676–88 Newton PM, Najabat-Lattif HF, Santiago G, Salvi A. The learning styles neuromyth is still thriving in medical education. Front Hum Neurosci 2021; 15: 708540 Follow the podcast Bluesky: @cardiacoutput.bsky.social X: @CardiacOutputMC If you've found this useful, a follow or a share genuinely helps other trainees find it — and do get in touch if there's a topic you'd like covered. This podcast is for medical education for healthcare professionals. It is not clinical advice.

    Cheap Knowledge, Scarce Experience: Training Generation Alpha

  2. Oct 23

    The Right Ventricle, Part 2: Function and Congestion

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

    The Right Ventricle, Part 2: Function and Congestion

  3. Oct 23

    The Right Ventricle, Part 1: Anatomy, Physiology and Views

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

    The Right Ventricle, Part 1: Anatomy, Physiology and Views

  4. Oct 19

    The Mitral Valve, Part 2: Grading Regurgitation and Stenosis

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

    The Mitral Valve, Part 2: Grading Regurgitation and Stenosis

  5. Oct 19

    The Mitral Valve, Part 1: Anatomy, Views and Mechanism

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

    The Mitral Valve, Part 1: Anatomy, Views and Mechanism

  6. Oct 18

    The Cath Lab Call: Anaesthesia for Primary PCI

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

    The Cath Lab Call: Anaesthesia for Primary PCI

  7. Oct 17

    Carcinoid Heart Disease: Ready for the Ventricle

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

    Carcinoid Heart Disease: Ready for the Ventricle

  8. Oct 13

    How Much Heparin on ECMO? (RATE)

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

    How Much Heparin on ECMO? (RATE)
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About

Cardiac Output is a podcast on cardiothoracic anaesthesia and intensive care medicine. Dr Mike Charlesworth and Dr Calum Downes bring you tacit knowledge from a national transplant and ECMO centre — the reasoning that never makes it into the textbook.

Information

  • Creator
    Dr Mike Charlesworth
  • Years Active
    2026
  • Episodes
    36
  • Rating
    Clean
  • Copyright
    © Copyright 2024 All rights reserved.
  • Show Website
    Cardiac Output

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