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"Severe aortic stenosis means a mean gradient over forty." Yet in one study of patients with true severe stenosis examined on TOE after induction, 54 per cent had a mean gradient under forty. General anaesthesia lowers the flow, and the gradient falls with it. This is part two of two on the aortic valve on transoesophageal echo, following the aortic valve chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. For aortic stenosis: calcific versus rheumatic valves, 2D versus 3D planimetry, colour as a screen, continuous-wave Doppler and its pitfalls (including mistaking a mitral jet), the severity grades, the continuity equation, the double envelope and the dimensionless index, and low-flow, low-gradient stenosis — true versus pseudo-severe, dobutamine, and the paradoxical form — plus the indications for surgery. For aortic regurgitation: causes in the leaflets and in the root, describing where a jet starts and where it goes, jet width, vena contracta and 3D vena contracta area, PISA and its limits, holodiastolic flow reversal in the descending aorta, pressure half-time, the severe thresholds, and the indications for surgery. Then endocarditis — vegetations, perforation, abscess and fistula — and obstruction below the valve: dynamic outflow obstruction and how to treat it, versus a fixed subaortic membrane or ridge. We finish with a round of grading, starting with an anaesthetised valve whose numbers say moderate. Chapters (00:00) Cold open — the gradient under forty (00:45) Causes of aortic stenosis (01:10) Calcific versus rheumatic valves (01:45) Planimetry in 2D and 3D (02:15) Associated findings (02:45) Colour Doppler (03:10) Peak velocity and mean gradient (04:15) Grading aortic stenosis (04:40) The continuity equation and the double envelope (06:05) The dimensionless index (06:30) Low-flow, low-gradient stenosis (07:20) True or pseudo-severe? (08:00) Paradoxical low-flow stenosis (08:40) Indications for surgery in AS (09:20) Causes of aortic regurgitation (10:10) Describing the jet (10:40) Jet width and vena contracta (11:50) PISA for the aortic valve (12:35) Flow reversal and pressure half-time (13:40) Indications for surgery in AR (14:15) Endocarditis (15:00) Outflow tract obstruction (16:15) Grading round Key takeaways General anaesthesia lowers flow and gradients: over half of true severe AS can have a mean gradient under 40 mmHg under GA — rely on the pre-op echo and flow-independent measures Calcific AS: heavy, asymmetric calcification and a star-shaped orifice; rheumatic: more commissural fusion and less calcium; no calcification makes significant AS very unlikely 3D planimetry at the leaflet tips correlates well with the continuity equation; 2D planimetry does not Use the highest of several CW velocities; beware an MR jet (usually >5 m/s, holosystolic, rounded) and use the long Bernoulli equation if LVOT velocity >1.5 m/s AS grades: mild 2.0–2.9 m/s, mean 4, AVA stays ≤1) from pseudo-severe (AVA rises >1) Paradoxical low-flow AS: normal EF, small thick LV, SVI 6 mm, EROA ≥0.30 cm², regurgitant volume ≥60 mL, regurgitant fraction ≥50% Holodiastolic flow reversal in the descending aorta with an end-diastolic velocity >20 cm/s is a sensitive sign of severe AR; PHT 200 ms suggests severe Endocarditis: vegetations on the ventricular side, perforation, abscess and fistula — check all the other valves Dynamic LVOT obstruction is late-peaking: fill, slow the heart, add a vasoconstrictor and stop inotropes; fixed subaortic stenosis peaks early with normally opening leaflets References / further reading The aortic valve and left ventricular outflow tract (Chapter 10). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686 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 Baumgartner H, Hung J, Bermejo J, et al. Recommendations on the echocardiographic assessment of aortic valve stenosis: a focused update from the EACVI and the ASE. J Am Soc Echocardiogr 2017; 30: 372–92 Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation. J Am Soc Echocardiogr 2017; 30: 303–71 Machida T, Izumo M, Suzuki K, et al. Value of anatomical aortic valve area using real-time three-dimensional transoesophageal echocardiography in patients with aortic stenosis. Eur Heart J Cardiovasc Imaging 2015; 16: 1120–8 Whitener G, McKenzie J, Akushevich I, et al. Discordance in grading methods of aortic stenosis by pre-cardiopulmonary bypass transesophageal echocardiography. Anesth Analg 2016; 122: 953–8 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.

Two numbers for the same aortic annulus: 23 mm on the 2D long-axis view, 27 mm on the 3D reconstruction — and the surgeon is sizing a valve. Neither number is wrong. This is part one of two on the aortic valve and left ventricular outflow tract on transoesophageal echo, built around the aortic valve chapter of the fourth edition of Practical Perioperative Transoesophageal Echocardiography. We start with the anatomy of the aortic root: the crown-shaped leaflet attachments, the sinuses of Valsalva and coronary origins, and the difference between the basal ring, the ventriculo-aortic junction and the functional aortic annulus — then the walls of the outflow tract and why the root's neighbours matter. Then the four standard views, how an off-axis short axis can fake a perforation, and where to find the coronary origins. The core of the episode is measuring the root properly: how to tell your long-axis view is truly centred, where to put the biplane cursor, which measurements are mid-systolic inner-edge and which are end-diastolic leading-edge, and why the annulus is an ellipse — with the 3D mean-diameter method for when the number really matters. Finally, the bicuspid aortic valve: prevalence, the Sievers classification, the elliptical orifice and doming, why a calcified bicuspid valve can be impossible to recognise, and why finding one should always make you look up at the aorta — plus unicuspid and quadricuspid valves. We finish with six measurement mistakes for Calum to spot. Part two covers stenosis, regurgitation, endocarditis and outflow tract obstruction. Chapters (00:00) Cold open — 23 or 27? (01:00) Why the aortic valve suits TOE (01:20) The aortic root and its crown (02:40) Where exactly is the annulus? (03:20) The outflow tract and neighbouring structures (04:10) The standard views and the coronaries (05:10) Measuring through the centre of the root (05:30) Checking you're on axis (06:10) Systole or diastole, inner or leading edge (06:35) The elliptical annulus and the mean diameter (07:40) Transgastric views and 3D (08:25) The bicuspid valve and its classification (09:25) Recognising a bicuspid valve — and looking up (10:20) Unicuspid and quadricuspid valves (10:45) Spot the error Key takeaways The aortic root runs from the ventriculo-aortic junction to the sinotubular junction; the leaflets attach in a crown shape, not a ring The basal ring is a virtual plane through the leaflet nadirs; the ventriculo-aortic junction sits slightly above it; the whole crown is the functional aortic annulus The non-coronary sinus lies next to the interatrial septum; the left and non-coronary leaflets are in continuity with the anterior mitral leaflet An off-axis short-axis view can fake a coaptation defect or perforation A centred long-axis view passes between the left and non-coronary cusps: a flat posterior root with no posterior leaflet or sinus; two sinuses and two leaflets mean you're off-axis In 3D biplane, place the short-axis cursor through the left/non-coronary commissure and the centre of the right coronary cusp Measure the LVOT and annulus in mid-systole, inner edge to inner edge; the sinuses, STJ and aorta at end-diastole, leading edge to leading edge The annulus is elliptical — axes can differ by up to 6 mm, and 3D measures larger than 2D; mean diameter = 2 × √(area ÷ π) Transgastric views give the only good Doppler alignment and see past shadowing from calcium or prostheses Bicuspid valves affect 0.5–2% of people (male:female about 3:1); left–right fusion is commonest; Sievers type 1 (one raphe) is over 90% Look for an elliptical systolic orifice and doming — and always measure the root and ascending aorta, and think about coarctation Unicuspid valves present young and go with aortopathy; quadricuspid valves usually leak and go with coronary anomalies References / further reading The aortic valve and left ventricular outflow tract (Chapter 10). In: Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025. ISBN 9780198873686 Charitos EI, Sievers HH. Anatomy of the aortic root: implications for valve-sparing surgery. Ann Cardiothorac Surg 2013; 2: 53–6 Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults. J Am Soc Echocardiogr 2015; 28: 1–39 Sievers HH, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg 2007; 133: 1226–33 Michelena HI, Della Corte A, Evangelista A, et al. International consensus statement on nomenclature and classification of the congenital bicuspid aortic valve and its aortopathy. Eur J Cardiothorac Surg 2021; 60: 448–76 Siu SC, Silversides CK. Bicuspid aortic valve disease. J Am Coll Cardiol 2010; 55: 2789–800 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.

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.

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.

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.

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 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.

"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.

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.

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.

A thirty-four-year-old for a hernia repair. After induction the pressure falls to fifty systolic, and the trainee reaches for adrenaline. The echo shows a thick septum, a tiny cavity and the mitral leaflet slapping into the outflow tract — and the pressure gets much worse. This episode is the cardiomyopathies: the main types, how they present, what they look like on echo, and why getting the label right changes what you do with your hands. We start with a definition and a simple way to hold the big three in your head — the ventricle that can't squeeze, the one that squeezes too well and won't relax, and the one that can't fill. Then each in turn. Dilated cardiomyopathy: the causes the exam wants, functional mitral regurgitation, apical thrombus, and the anaesthetic plan for a patient with a failing, afterload-sensitive ventricle, including devices and SGLT2 inhibitors. Hypertrophic cardiomyopathy: diagnosis, systolic anterior motion and the dagger-shaped outflow signal, why the anaesthetic goals run opposite to almost everything else we do, and what mavacamten means for theatre. Restrictive cardiomyopathy: amyloid, the low-voltage ECG with thick walls, and apical sparing on strain. Then the mimic that matters — constrictive pericarditis versus restriction, why telling them apart is the difference between a curable and an incurable disease, the echo and cath lab discriminators, and the handbook's rules for a pericardiectomy. We finish with arrhythmogenic right ventricular cardiomyopathy and takotsubo, which can obstruct too. The wrap-up is an echo spot-test: six pictures, six diagnoses — and six different treatments for the same low blood pressure. Chapters (00:00) Cold open — the wrong drug for a thick heart (00:40) Definition and classification (01:50) Dilated cardiomyopathy: causes, presentation and echo (03:20) Ischaemic or non-ischaemic? (03:40) Anaesthesia for dilated cardiomyopathy (05:15) Hypertrophic cardiomyopathy: presentation and echo (06:40) When is it obstructive? (07:15) Anaesthetic goals in obstruction (08:10) Long-term treatment, including mavacamten (08:40) Restrictive cardiomyopathy and amyloid (10:15) Strain imaging and apical sparing (10:50) Constrictive pericarditis: the mimic (11:30) Telling constriction from restriction (12:50) Anaesthesia for pericardiectomy (13:30) Arrhythmogenic right ventricular cardiomyopathy (14:25) Takotsubo (15:25) Echo spot-test Key takeaways A cardiomyopathy is disease of the heart muscle not explained by coronary, hypertensive, valvular or congenital disease Dilated: can't squeeze — big round ventricle, functional MR, apical thrombus risk; avoid tachycardia and negative inotropy; it tolerates a modest fall in afterload Turn off ICD shock therapies for diathermy, and stop SGLT2 inhibitors before surgery (euglycaemic ketoacidosis) Hypertrophic: wall ≥15 mm (≥13 mm with family history); obstruction is a gradient ≥30 mmHg, significant at ≥50 In obstruction, fill them, slow them, use phenylephrine or vasopressin, and stop the inotropes — adrenaline can be fatal Mavacamten lowers contractility and can push the ejection fraction down — know if your patient is on it Restrictive: can't fill — big atria, normal ventricles, restrictive filling and a low e′; amyloid gives thick walls, a low-voltage ECG and apical sparing Constriction is curable: septal bounce, respiratory variation in mitral inflow, preserved e′ (lateral lower than septal) and discordant ventricular pressures Pericardiectomy: no PEEP, vasopressors running before induction, and be ready to open the chest early ARVC: young athlete, VT with a left bundle pattern, T-wave inversion V1–V3 and epsilon waves; takotsubo can obstruct the outflow tract Echo before the inotrope — the same hypotension has different treatments depending on the ventricle References / further reading Arbelo E et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J 2023; 44: 3503–626 Ommen SR et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy. Circulation 2024; 149: e1076–e1126 Garcia MJ. Constrictive pericarditis versus restrictive cardiomyopathy? J Am Coll Cardiol 2016; 67: 2061–76 Ghadri JR et al. International expert consensus document on takotsubo syndrome (part I). Eur Heart J 2018; 39: 2032–46 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.

Day one after mitral valve surgery. The monitor says the cardiac index is a healthy three point two. The lactate is six, the feet are cold and the urine has stopped. One of those numbers is lying — and it isn't the lactate. This episode is cardiac output monitoring, for the exam and for the bedside: how each device works, the physiology underneath, when we actually use them, and where each one misleads you. We start with first principles: cardiac output as heart rate times stroke volume, the exam definitions of preload, afterload and contractility, and why a normal blood pressure can hide a failing pump. Then the Fick principle, what a central venous saturation can and can't tell you, and how to diagnose a low-output state by looking at the whole patient rather than one number. Then the devices, one by one. The pulmonary artery catheter — Stewart–Hamilton thermodilution, the continuous thermal-filament version, floating one by the waveforms, complications, the evidence from ESCAPE and PAC-Man, and why it's still the only monitor that shows you the right heart and the pulmonary circulation directly. PiCCO and LiDCO, and their volumetric extras. Uncalibrated pulse contour monitors, and the arrhythmias, valve leaks, vasoplegia and balloon pumps that break them. Stroke volume and pulse pressure variation, and why an open chest and a failing right ventricle make them unreliable. The oesophageal Doppler — the four assumptions behind its number. Echo, which gives you not just the number but the reason. Bioimpedance, and why it never caught on. And what the console really tells you on ECMO, a BiVAD or an implanted LVAD. We finish with a quick-fire quiz, so you can test yourself on the lot. Chapters (00:00) Cold open — one of these numbers is lying (00:50) The physiology: stroke volume, pressure and flow (01:50) The Fick principle and venous saturations (02:55) Diagnosing low output at the bedside (03:55) The pulmonary artery catheter and thermodilution (05:55) Floating a PA catheter by the waveforms (07:25) Complications and the evidence (09:05) Transpulmonary thermodilution — PiCCO (10:20) Lithium dilution — LiDCO (10:55) Uncalibrated pulse contour monitors (12:00) Stroke volume and pulse pressure variation (12:55) The oesophageal Doppler and its assumptions (15:30) Echo: the number and the reason (16:20) Bioimpedance and bioreactance (16:55) Flow on ECMO, BiVADs and LVADs (17:35) Putting it together (18:05) Quick-fire quiz Key takeaways Cardiac output = heart rate × stroke volume; mean arterial pressure = cardiac output × SVR — so a normal pressure says nothing about which one is holding it up Central venous saturation is not truly mixed venous, and it can mislead in both directions — low for reasons other than output, and high when the tissues can't extract oxygen Diagnose low output from the whole patient: symptoms, signs, end-organ function, lactate and acidosis The PA catheter is the reference standard (Stewart–Hamilton thermodilution); continuous versions use a thermal filament and lag behind sudden change Know the waveforms — RA 0–8, RV 15–30/0–8, PA 15–30/4–12, wedge ~12 mmHg; never leave the balloon wedged; beware existing left bundle branch block ESCAPE and PAC-Man showed no routine survival benefit — use it where the numbers will change what you do PiCCO adds global end-diastolic volume and extravascular lung water, but needs regular recalibration; any thermodilution is unreliable on ECMO Uncalibrated pulse contour is good for trends, poor in AF, aortic regurgitation, vasoplegia, a damped line or a balloon pump SVV/PPV above ~12–13% predicts fluid responsiveness only in a fully ventilated, closed-chest patient in sinus rhythm Oesophageal Doppler assumes a nomogram aortic area, a fixed 70:30 split, the right vessel at a sensible angle, and laminar flow; normal FTc 330–360 ms Echo stroke volume = LVOT area × VTI — the diameter is squared, so small errors grow; its real value is telling you why the output is low On ECMO or a BiVAD the console shows circuit flow only; an LVAD estimates flow from power and speed References / further reading Binanay C et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005; 294: 1625–33 Harvey S et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005; 366: 472–7 Marik PE et al. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med 2009; 37: 2642–7 Cecconi M et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014; 40: 1795–815 Teboul JL et al. Less invasive hemodynamic monitoring in critically ill patients. Intensive Care Med 2016; 42: 1350–9 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.

Forty minutes into an aortic valve replacement, the cross-clamp is on and the heart is arrested. Then a little electrical activity starts creeping back on the ECG. What do you do? Tell the surgeon — out loud, straight away — because that heart is waking up while it's still ischaemic. The anaesthetist is part of myocardial protection, even though the solution runs through the perfusionist's pump. This episode is cardioplegia from the top end of the table. We start with why it exists: the moment the aorta is clamped, the heart has no coronary flow, and a warm, beating, ischaemic heart runs out of energy in minutes. Cardioplegia makes planned ischaemia survivable in five ways — arrest, cool, empty, feed and buffer, and limit reperfusion injury — and arrest does most of the work. Then what's in the bag, grouped the way examiners like it: an arresting agent, buffers, osmotic agents and substrate. How potassium produces a depolarised arrest by inactivating fast sodium channels, and why that isn't quite a resting membrane. Why the commonest solution is 4:1 blood cardioplegia, and what blood adds over crystalloid. Warm versus cold as a real trade-off — and the hot shot that gets the heart ready before the clamp comes off. Delivery routes next. Antegrade into the aortic root as standard, direct into the ostia, or down the vein grafts. Retrograde through the coronary sinus for aortic regurgitation, aortic and root surgery, and severe coronary disease — with the 40 mmHg limit on coronary sinus pressure, why retrograde protects the right ventricle less well, and how to confirm the cannula on TOE. And why antegrade into a regurgitant root distends the ventricle instead of perfusing it. Then the seven complications — trauma, air, oedema, bleeding, difficulty restarting, electrolyte disturbance and inadequate protection — and how the last one really shows up: as a heart that comes off badly. del Nido, with its single long-acting dose, lidocaine and low calcium. Custodiol (HTK), which arrests the heart by taking the sodium away rather than adding potassium, and the price you pay in volume and dilution. And Laplace's law, which explains why a distended ventricle is dangerous and why we vent — during surgery, with a balloon pump, and on VA-ECMO. We finish with the anaesthetist's checklist during the cross-clamp, and what to be ready for when it comes off. Chapters (00:00) Cold open — the ECG wakes up during the cross-clamp (01:00) Why we need cardioplegia, and the five mechanisms (01:50) How much oxygen arrest and cooling save (02:30) What's in the bag (02:40) Potassium and the depolarised arrest (04:10) Buffers, osmotic agents and substrate (04:50) Blood versus crystalloid (05:40) Warm versus cold (06:30) The hot shot (07:00) Antegrade delivery (07:40) Retrograde delivery, and when you need it (08:00) Why antegrade fails with aortic regurgitation (08:40) The coronary sinus pressure limit, and the right ventricle (09:20) Confirming the retrograde cannula on TOE (10:00) The seven complications (12:20) del Nido (13:30) Custodiol (HTK) (15:00) Laplace's law, and why we vent (16:00) The anaesthetist's checklist during the cross-clamp (16:30) Wrap-up Key takeaways If electrical activity returns on the ECG during the cross-clamp, tell the surgeon straight away — the heart is working while ischaemic Cardioplegia protects the heart in five ways: arrest, cool, empty, deliver substrate and buffering, and limit reperfusion injury — arrest does the heavy lifting Contents fall into four groups: an arresting agent (usually potassium, with magnesium), buffers, osmotic agents and substrate High potassium raises the resting membrane potential and inactivates fast sodium channels — a depolarised arrest in diastole Blood cardioplegia (4:1) adds oxygen carriage, buffering, free-radical scavenging and better microvascular flow, with less oedema Cold maximises metabolic suppression; warm supports aerobic metabolism; a warm "hot shot" before clamp removal prepares the heart for reperfusion Retrograde delivery via the coronary sinus is used for significant aortic regurgitation, aortic valve and root surgery, and severe coronary disease — keep sinus pressure below 40 mmHg Retrograde protects the right ventricle less well, so it's often combined with antegrade In aortic regurgitation, antegrade root delivery distends the left ventricle — watch the LV on TOE and say if it's getting bigger Complications: trauma, air, myocardial oedema, bleeding, difficulty restarting, systemic electrolyte disturbance and inadequate protection del Nido (1 part blood to 4 crystalloid, with lidocaine and low calcium) gives a single dose lasting up to around 90 minutes Custodiol (HTK) arrests by sodium depletion — a hyperpolarised arrest — with long protection, but large volumes cause haemodilution and hyponatraemia Laplace: wall tension rises with pressure and radius — which is why distension is dangerous and why we vent Solutions, doses and protocols are Wythenshawe-specific — check your own unit's practice References / further reading Gravlee GP et al., eds. Cardiopulmonary Bypass and Mechanical Support: Principles and Practice, 4th edn. Philadelphia: Wolters Kluwer, 2016 Matte GS, del Nido PJ. History and use of del Nido cardioplegia solution at Boston Children's Hospital. J Extra Corpor Technol 2012; 44: 98–103 Edelman JJB et al. Custodiol for myocardial protection and preservation: a systematic review. Ann Cardiothorac Surg 2013; 2: 717–28 Mackay JH, Arrowsmith JE et al., eds. Core Topics in Cardiac Anaesthesia, 3rd edn. Cambridge: Cambridge University Press, 2020 — myocardial protection chapter 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. Solutions, doses and practice described reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.

Eight o'clock ward round, day two after a coronary artery bypass, and the monitor shows atrial fibrillation at a hundred and fifty. Calum's answer is amiodarone — and that is the single most common wrong answer on the unit. Not because amiodarone is wrong, but because of where it sits in the order. This is atrial fibrillation on the cardiothoracic intensive care unit, top to bottom. And it matters beyond the bedside: in a recent Fellowship paper it was the worst-performing question on the whole exam, with a pass rate of about 43 per cent. The examiners were specific about where candidates fell down — the management, and the anaesthetic for elective DC cardioversion. The bit everyone assumes is easy. We start with how common it is — about a third of patients after coronary surgery, up to half after valve or combined procedures, peaking on days two and three — and why it isn't benign. Then a framework you can use on a ward round: substrate and trigger. The substrate is atrial; the triggers are catecholamines, pain, hypovolaemia, hypoxia, anaemia, electrolytes and the inflammatory response to bypass. Almost every trigger is something you can change. Then the four strands of management — rhythm, rate, recurrence and thromboembolism — and the step that comes before all of them. Correct the physiology first: potassium, magnesium, pain, volume; exclude tamponade and pneumothorax with a scan and a film, not a glance at the drain; look for sepsis; and check for a misplaced epicardial pacing wire irritating the atrium. Only then a drug. Amiodarone as the workhorse — why it acts on both rhythm and rate, and why the slow loading dose is a safety feature rather than fussiness in a shocked post-cardiotomy patient. Then the drugs we avoid, and the specific reason for each: digoxin, verapamil and diltiazem, flecainide and the lesson of the CAST trial, beta-blockers (and why esmolol if you must), and adenosine as a diagnostic rather than a treatment. Plus the Vaughan Williams classification in ninety seconds, and when an unstable patient needs a synchronised shock rather than a drug. Anticoagulation next: our local position on new-onset post-operative AF and the reasoning behind it, anticoagulant mechanisms and reversal agents, the case for and against the direct oral anticoagulants, and neuraxial timings. Then a trap specific to cardiac surgery — andexanet alfa can look exactly like heparin resistance on bypass, which is why you tell the perfusionist before you reverse, not afterwards. We finish with the section the examiners said was done worst — the anaesthetic for a DC cardioversion list, including what to avoid and the bailout you set up before the first patient — and the long-term options for rhythm, rate and stroke prevention. Chapters (00:00) Cold open — AF at 150, and the commonest wrong answer (00:50) Why this was the worst-answered exam question (01:20) Incidence, and why it isn't benign (02:10) Substrate and trigger (02:40) Causes of AF in general (03:30) The four strands of management (03:50) Correct the physiology first (04:20) The misplaced pacing wire (04:50) Amiodarone, and why the slow load matters (06:30) The drugs we avoid — and why (08:00) The Vaughan Williams classification (08:50) The unstable patient (09:20) Anticoagulation: our local position (10:00) Mechanisms and reversal (11:00) For and against the DOACs (11:30) Neuraxial timings (11:50) Reversal before bypass — andexanet and apparent heparin resistance (13:10) Anaesthesia for DC cardioversion (14:30) Long-term rhythm, rate and stroke prevention (15:10) Wrap-up Key takeaways Post-operative AF affects about a third of patients after CABG and up to half after valve or combined surgery, peaking on days two to three — often self-terminating, but not benign Think substrate (atrial trauma, inflammation, stretch, fibrosis, a large left atrium) and trigger (catecholamines, pain, hypovolaemia, hypoxia, anaemia, electrolytes, the inflammatory response) Four strands of management: restore rhythm, control rate, prevent recurrence, prevent thromboembolism Correct the physiology first: K⁺ 4.5–5.5, Mg²⁺ above 1.0, treat pain and hypovolaemia, exclude tamponade and pneumothorax, look for sepsis, and check the pacing wires Amiodarone 300 mg over 20–60 minutes (never as a rapid bolus), centrally where possible, then 600–900 mg over 24 hours — rapid loading causes negative inotropy and vasodilation Digoxin is not an acute agent; verapamil and diltiazem are negatively inotropic; flecainide is contraindicated in structural heart disease and ischaemia (the CAST lesson); esmolol if you must beta-block; adenosine is diagnostic, not therapeutic Adverse features — shock, syncope, myocardial ischaemia, heart failure — mean synchronised DC cardioversion, not a drug; know the Resuscitation Council adult tachycardia algorithm Know anticoagulants by mechanism, because reversal follows mechanism Reversing a DOAC before bypass? Tell the surgeon and the perfusionist first — andexanet sequesters heparin–antithrombin and mimics heparin resistance Cardioversion list: pre-oxygenate, titrate propofol, support the airway with spontaneous ventilation, avoid midazolam, volatiles and TCI, and set out the bailout (rocuronium, intubation, sugammadex) before you start Doses, thresholds and anticoagulation practice are Wythenshawe-specific — check your own guidelines References / further reading Resuscitation Council UK. Adult tachycardia algorithm. Resuscitation Guidelines 2021 Van Gelder IC et al. 2024 ESC Guidelines for the management of atrial fibrillation. Eur Heart J 2024 National Institute for Health and Care Excellence. Atrial fibrillation: diagnosis and management (NG196). 2021 Echt DS et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo: the Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991; 324: 781–8 Horlocker TT et al. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: ASRA evidence-based guidelines (4th edition). Reg Anesth Pain Med 2018; 43: 263–309 Royal College of Anaesthetists. Final FRCA written examination — chair's reports 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. Medications, doses and practice described reflect local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.

Last episode we put a probe on the chest. This one goes down the oesophagus — and it starts somewhere uncomfortable. Inserting a transoesophageal probe is something we do to a patient that can cause them significant harm. Maybe once a year, sometimes more, a patient comes to harm because an anaesthetist put a probe down. We do a great many of these, so it is not unreasonable to think we sometimes cause damage and never find out. But sometimes the injury is severe: an oesophageal tear, upper gastrointestinal bleeding. Severe harm runs at roughly one in two thousand, from a UK audit by the Association of Cardiothoracic Anaesthetists, with female sex, steroid use and a low body mass index as risk factors — all observational, so hold it loosely. And then the argument that follows from it. Contraindications are genuinely hard to find, and Mike's position has changed over time: transoesophageal echo should be mandatory for essentially all cardiac surgery unless there is a good reason not to. Not because every operation demands it, but because of what turns up — valvular problems and dissections in patients listed for bypass grafts with supposedly normal hearts, things that would never have been found without scanning them on the table. From there, the practical half. Three ways to get an ejection fraction, in ascending order of rigour: the eyeball, which in experienced hands correlates well and is what you'll actually use in a crashing patient; fractional area change from the transgastric short axis; and Simpson's biplane, the most rigorous and the most dependent on an endocardial border you can genuinely see. Garbage in, garbage out. Then the right ventricle, and an argument worth having: there are many accepted ways to assess it, and the very existence of so many tells you that none is good enough alone. Watch TAPSE being measured in theatre and ask honestly whether that is a precise, scientific number — particularly off-axis on a transoesophageal probe. Most of the time what you are doing is judging performance by eye and following the trend: how it looked before, how it looks now, what you did in between, and whether it worked. Plus the levers when the right ventricle is struggling — rate and rhythm, preload, afterload, contractility and coronary perfusion, and what comes after them. Systolic anterior motion gets done properly this time, and the key idea is that echo lets you predict it rather than just diagnose it: a long anterior mitral leaflet, a small hypertrophied ventricle with a narrow outflow tract, and a short coaptation-to-septum distance. Then the management, which runs almost exactly opposite to instinct. Then the probe as a theatre instrument. Siting a balloon pump tip just distal to the subclavian — and what goes wrong if it sits too high or too low. The Protek Duo, and why its tip must sit beyond the pulmonary valve. And the rule worth carrying out of the whole topic: any patient on mechanical support with haemodynamic instability does not have to do very much to earn a scan. The section Mike calls most underrated is the one where you help the surgeon and the perfusionist. The venous drainage cannula that has slipped into a hepatic vein — presenting as low flows and poor drainage that everyone assumes is volume — and the non-standard view that finds it. Confirming the retrograde cardioplegia cannula in the coronary sinus, which protects the heart for the entire operation. And watching the wires: the femoral venous wire in peripheral bypass, and the balloon pump wire in the descending aorta, with a live commentary nobody else in the room can give. We finish with transplantation — what is and isn't useful to scan, why a heart that has just been ischaemic cannot be judged like a normal one, and the three questions all of this monitoring exists to answer before you take that patient out to the unit. Chapters (00:00) Cold open — the probe can hurt people (01:00) One in two thousand, and the risk factors (01:40) Contraindications, and how few there are (02:20) Who should get one — and why the answer changed (03:20) Accreditation for cardiac anaesthetists (03:50) Ejection fraction: eyeball, FAC and Simpson's biplane (05:00) The right ventricle, and why so many methods is a warning (06:20) The levers when the right ventricle is failing (07:00) Predicting systolic anterior motion before it happens (08:00) Treating it when it happens (08:40) Siting a balloon pump (09:20) The Protek Duo (10:10) Instability on support earns a scan (11:00) Which pipes you can actually see (11:50) Helping the surgeon: the cannula in the hepatic vein (12:50) Confirming retrograde cardioplegia in the coronary sinus (13:20) Watching the wires (13:50) Transplantation (15:00) Wrap-up Key takeaways Putting a probe down can seriously harm a patient: severe harm is around 1 in 2000, with female sex, steroids and low BMI as observational risk factors Contraindications are few — oesophageal pathology or swallowing difficulty, and a pharyngeal pouch is difficult but not absolute TOE should be mandatory for essentially all cardiac surgery unless there's a good reason not to, because we find valve lesions and dissections in hearts we believed were normal Ejection fraction three ways: visual estimation, fractional area change from the transgastric short axis, and Simpson's biplane — the most rigorous and the most dependent on image quality The number of accepted methods for assessing the right ventricle is itself evidence that none is good enough alone — use the trend and your eyes When the right ventricle struggles, work the levers: rate and rhythm, preload, afterload, contractility, coronary perfusion — then mechanical support Predict systolic anterior motion before bypass comes off: long anterior mitral leaflet, small hypertrophied ventricle, narrow outflow tract, short coaptation-to-septum distance Treat it by filling, decreasing the rate, stopping the inotropes and adding a vasoconstrictor Balloon pump tip just distal to the left subclavian: too high risks the arm and brain vessels, too low risks the mesenteric and renal arteries and won't augment properly The Protek Duo tip belongs beyond the pulmonary valve, in the pulmonary artery Any patient on mechanical support with haemodynamic instability earns a transoesophageal echo — look at flows, septal position, ventricular size and the position of the pipes A venous drainage cannula that has slipped into a hepatic vein presents as low flows and poor drainage that everyone assumes is volume — and one non-standard view finds it Confirming the retrograde cardioplegia cannula in the coronary sinus protects the heart for the whole operation A freshly transplanted, recently ischaemic heart has a fixed stroke volume, is highly rate-dependent and is on inotropes — you are interpreting a picture that is abnormal by design Everything you are monitoring answers one of three questions: is this patient stable, in a low cardiac output state, or sliding into one? References / further reading Association of Cardiothoracic Anaesthesia and Critical Care. UK audit of transoesophageal echocardiography probe-related injury Lambert AS, Allen SJ, Sidhu S, eds. Practical Perioperative Transoesophageal Echocardiography, 4th edn. Oxford: Oxford University Press, 2025 Hahn RT et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr 2013 European Association of Cardiovascular Imaging / EACTAIC. Transoesophageal echocardiography certification British Society of Echocardiography. Transoesophageal echocardiography accreditation 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. Practice described reflects local Wythenshawe practice at the time of recording — always follow your own centre's guidelines and current local policy.