Audience: echocardiographers, cardiologists and acute physicians. Evidence reviewed: September 2026.

Key message

A left-atrial mass attached near the fossa ovalis is suggestive of myxoma, but attachment, mobility, vascularity and clinical context must be defined before diagnosis. Important mimics include thrombus, other tumours, vegetation and extracardiac compression. Once a probable myxoma is identified, prompt specialist surgical assessment is usual because embolic and obstructive complications can be sudden.

Clinical presentation

• Obstruction: exertional dyspnoea, orthopnoea, syncope or positional symptoms from intermittent mitral inflow obstruction.
• Embolism: cerebral, coronary, retinal or systemic arterial events.
• Constitutional features: fever, weight loss, raised inflammatory markers and anaemia.
• Incidental discovery: an asymptomatic mass found during unrelated imaging.

Echocardiographic assessment

Transthoracic echocardiography is the usual first test. Record the mass in multiple planes and describe size, shape, surface, mobility, stalk, precise attachment and relationship to the mitral valve and pulmonary veins. Assess functional mitral obstruction with Doppler at a stated heart rate, associated regurgitation, chamber size, pulmonary-pressure probability and pericardial effusion.

Transoesophageal echocardiography improves definition of attachment, small lesions and surgical anatomy. Three-dimensional echo may clarify the stalk and spatial relationship. Avoid declaring histology from echogenicity alone.

When CT or CMR helps

CMR can assess tissue signal, perfusion and enhancement; CT defines calcification, coronary anatomy and extracardiac disease. Neither modality removes the need for pathology. If malignancy or thrombus remains plausible, imaging and treatment decisions should be coordinated across cardiology, radiology, oncology/infectious diseases and surgery as relevant.

Management

Probable cardiac myxoma is generally referred promptly for surgical excision, including the attachment site where feasible. Urgency reflects mobility, prior embolism, obstruction, tumour size and clinical stability. Coronary assessment follows age, symptoms and surgical protocol; tumour neovascularisation may occasionally be demonstrated.

Histopathology confirms the diagnosis. Follow-up echocardiography checks for recurrence, which is uncommon after complete excision but more likely in familial syndromes, multiple tumours or incomplete resection. Younger patients, multiple or recurrent myxomas, or suggestive endocrine/skin features should prompt consideration of Carney complex and genetic assessment.

Selected references

• Cardiac myxomas: a narrative review. J Cardiothorac Surg. 2025.
• Open-access 2025 review of cardiac myxomas.
• ASE comprehensive transthoracic echocardiography guideline.

Educational material only. A suspected intracardiac tumour or thrombus requires timely specialist assessment; acute obstruction or embolism is an emergency.

Audience: acute-cardiology, interventional-cardiology and cardiothoracic teams. Evidence reviewed: September 2026.

Key message

In acute coronary syndrome (ACS), culprit treatment and complete revascularisation are related but distinct decisions. CABG should remain in the index-admission pathway when anatomy, diabetes, ventricular dysfunction, mechanical complications or PCI feasibility suggests a prognostic or technical advantage—provided timing balances recurrent-ischaemia and bleeding risks.

Stabilise first, then define the problem

Immediate management follows ACS severity: resuscitation, antithrombotic therapy, urgent angiography and culprit reperfusion when indicated. Cardiogenic shock, ongoing ischaemia, failed PCI or a mechanical complication demands rapid multidisciplinary escalation; the ideal revascularisation mode may differ from that in a stable NSTEMI patient.

Anatomy that should trigger surgical discussion

• Significant left-main disease, especially complex distal bifurcation disease.
• Complex three-vessel disease not amenable to durable complete PCI.
• Diabetes with multivessel coronary disease where long-term evidence favours surgery in suitable patients.
• Need for concomitant valve, aortic or mechanical-complication surgery.
• Failed or complicated PCI with ongoing jeopardised myocardium.

The index-admission Heart Team

Timing is an individual risk balance

Emergency CABG may be necessary for failed reperfusion, anatomy unsuitable for PCI with ongoing ischaemia, or mechanical complications. In stable patients, surgery is often delayed sufficiently to reduce perioperative bleeding and allow antiplatelet washout, but unnecessary discharge can expose patients to recurrent ischaemia and fragmented decision-making. The plan should state the reason for timing, antithrombotic strategy and triggers for acceleration.

Routine platelet-transfusion or bridging strategies should not be improvised. Follow the current guideline, local surgical protocol and patient-specific thrombotic and bleeding risks. Aspirin is commonly continued, while interruption intervals for P2Y12 inhibitors depend on the agent and urgency.

Communication standard

Document: culprit and residual anatomy; whether PCI achieved stable reperfusion; why CABG, PCI or medical therapy is preferred; estimated surgical and bleeding risk; antiplatelet stop dates; intended timing; contingency plan; and the patient’s informed preference. “For outpatient discussion” is not an adequate plan when prognostically important disease remains untreated.

Selected references

• 2025 ACC/AHA multisociety guideline for acute coronary syndromes.
• 2025 ACS guideline full publication.
• 2023 ESC acute coronary syndromes guideline.

Educational material only. Revascularisation strategy and timing require case-specific Heart Team decisions and current local antithrombotic/surgical protocols.

Audience: heart-failure clinicians, general physicians and trainees. Evidence reviewed: September 2026.

Key message

Digoxin remains useful for selected patients, but it is not a foundational mortality-reducing therapy for heart failure. Its narrow therapeutic index makes indication, renal function, dose, drug interactions and clinical monitoring inseparable from prescribing.

Two distinct indications

Evidence in HFrEF

In the Digitalis Investigation Group trial, digoxin did not reduce all-cause mortality but reduced hospital admission for worsening heart failure. The trial pre-dated angiotensin-receptor neprilysin inhibitors, SGLT2 inhibitors and widespread modern device therapy, so absolute benefits in present practice are uncertain. Contemporary guidelines therefore position digoxin as an option for selected symptomatic HFrEF rather than routine foundational treatment.

Choosing and monitoring treatment

• Confirm the goal: symptom/hospitalisation reduction or ventricular-rate control.
• Use a low maintenance dose tailored to age, lean body mass and renal function; loading is rarely needed in stable chronic care.
• Check renal function and potassium before treatment and after clinically important changes.
• Review interacting medicines, including amiodarone, verapamil, macrolides and other P-glycoprotein inhibitors.
• If a serum concentration is required, sample at steady state and at least 6–8 hours after the last dose; interpret the result with symptoms, ECG and renal function.

For heart failure, many experts aim for a low serum concentration, commonly 0.5–0.9 ng/mL, when measurement is clinically indicated. A number within a laboratory “therapeutic range” does not exclude toxicity, particularly in older adults, renal impairment, hypokalaemia, hypomagnesaemia or hypothyroidism.

Recognising toxicity

Toxicity may cause anorexia, nausea, confusion, visual disturbance, bradyarrhythmia, atrioventricular block or almost any tachyarrhythmia. Stop digoxin, obtain an ECG, electrolytes, renal function and an appropriately timed level, and assess severity urgently. Life-threatening arrhythmia or significant hyperkalaemia may require digoxin-specific antibody fragments under emergency/toxicology guidance.

When to reconsider

Reassess digoxin when renal function changes, interacting therapy is added, bradycardia develops, the original indication disappears or adherence/monitoring is unreliable. Withdrawal may worsen symptoms or rate control in some patients, so deprescribing should be planned rather than automatic.

Selected references

• The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997.
• 2026 ESC guideline for acute and chronic heart failure.
• 2022 AHA/ACC/HFSA heart-failure guideline.

Educational material only. Dose and monitoring must follow the current product information, renal function, local formulary and individual clinical context.

Audience: cardiology clinicians and trainees. Evidence reviewed: September 2026.

Key message

In symptomatic obstructive hypertrophic cardiomyopathy (HCM), first confirm that dynamic left-ventricular outflow-tract (LVOT) obstruction explains the symptoms. Treatment then proceeds from physiology-aware medical therapy to specialist myosin-inhibitor or septal-reduction strategies, while sudden-death risk is assessed on a separate track.

1. Confirm the phenotype and mechanism

• Document maximal wall thickness, distribution of hypertrophy and LV systolic/diastolic function.
• Identify systolic anterior motion, mitral–septal contact and the mechanism/severity of mitral regurgitation.
• Measure resting and provoked LVOT gradients with correctly aligned CW Doppler. Exercise stress echocardiography is valuable when symptoms and resting/Valsalva gradients disagree.
• Use CMR for anatomy, apical disease, scar burden and alternative diagnoses.
• Exclude important mimics and contributors such as hypertension, valve disease, coronary disease, anaemia and arrhythmia.

2. Define what limits the patient

Record NYHA class, exertional chest pain, presyncope/syncope, palpitations and exercise capacity. Review volume status, blood pressure and drugs that reduce preload or afterload. New atrial fibrillation can sharply worsen filling and symptoms and requires prompt rhythm/rate and anticoagulation assessment.

3. Start physiology-directed treatment

A non-vasodilating beta-blocker is generally first-line for symptoms attributable to obstruction. Verapamil or diltiazem may be considered when beta-blockers are ineffective or not tolerated, but caution is required with hypotension, severe obstruction or advanced congestion. Disopyramide can reduce obstruction when added under expert supervision, with attention to anticholinergic effects and QT prolongation.

4. Escalate persistent severe symptoms

Patients with substantial symptoms despite maximally tolerated therapy should be referred to an experienced HCM centre. Options include a cardiac myosin inhibitor and septal reduction. Surgical myectomy is preferred when concomitant cardiac surgery or complex mitral/subvalvular anatomy requires correction. Alcohol septal ablation is an alternative for selected anatomy and risk profiles. Operator and centre experience materially affect outcomes.

5. Run parallel risk pathways

Sudden-cardiac-death risk assessment is not replaced by symptom control or gradient reduction. Evaluate previous cardiac arrest or sustained ventricular tachycardia, unexplained syncope, family history, maximal wall thickness, apical aneurysm, LV systolic dysfunction, non-sustained ventricular tachycardia and CMR scar within the applicable guideline framework. Also address genetics and family screening, atrial fibrillation, stroke prevention, pregnancy, exercise and endocarditis advice.

Selected references

• 2024 AHA/ACC multisociety HCM guideline.
• 2024 HCM guideline—PubMed record.
• 2023 ESC cardiomyopathy guideline.

Educational material only. Myosin-inhibitor and septal-reduction decisions require specialist HCM-centre assessment and current local prescribing guidance.

Audience: heart-failure clinicians, trainees and evidence-based-medicine readers. Evidence reviewed: September 2026.

Bottom line

FINEARTS-HF showed that finerenone reduced the rate of the composite of total worsening heart-failure events and cardiovascular death in symptomatic heart failure with left-ventricular ejection fraction (LVEF) ≥40%. The benefit was driven mainly by fewer worsening heart-failure events, with more hyperkalaemia but less hypokalaemia.

Clinical question

Does the non-steroidal mineralocorticoid-receptor antagonist finerenone improve outcomes in patients with heart failure and mildly reduced or preserved ejection fraction?

Design and population

FINEARTS-HF was an international, double-blind, randomised, placebo-controlled trial. It enrolled 6,001 patients aged 40 years or older with symptomatic heart failure, LVEF ≥40%, structural heart disease and elevated natriuretic peptides. Participants received finerenone or placebo in addition to usual therapy. The primary endpoint was a recurrent-event composite: total worsening heart-failure events plus cardiovascular death.

Results

During a median follow-up of 32 months, 1,083 primary-outcome events occurred in the finerenone group and 1,283 in the placebo group. The rate ratio was 0.84 (95% confidence interval 0.74–0.95; P=0.007). Worsening heart-failure events numbered 842 versus 1,024 (rate ratio 0.82, 95% CI 0.71–0.94). Cardiovascular death occurred in 8.1% versus 8.7% of participants; the trial did not demonstrate a clear mortality reduction.

Treatment effects were broadly consistent across prespecified subgroups, including the range of LVEF studied. Finerenone increased creatinine and hyperkalaemia risk but reduced hypokalaemia. The clinical trade-off therefore includes renal-function and potassium surveillance.

Strengths and limitations

• Strengths: large randomised design, blinded outcome assessment, broad geography and clinically meaningful recurrent-event endpoint.
• Endpoint interpretation: the primary benefit was morbidity rather than proven cardiovascular survival.
• Generalisability: trial eligibility and monitoring may not represent frail patients, advanced kidney disease or routine-care adherence.
• Background therapy: evolving SGLT2-inhibitor use complicates direct extrapolation to every present-day regimen.

Clinical application

Finerenone is a disease-modifying option for appropriately selected patients with HFmrEF/HFpEF, particularly when recurrent decompensation risk is important. Before initiation, confirm the indication, estimated glomerular filtration rate, serum potassium, interacting medicines and the ability to repeat blood tests. Do not assume interchangeability with spironolactone or eplerenone: molecular properties, evidence bases and licensed indications differ.

Selected references

• Solomon SD et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024.
• FINEARTS-HF primary publication.
• 2026 ESC guideline for acute and chronic heart failure.

Educational critical appraisal only. Prescribing must follow the current licence, formulary, renal/potassium criteria and local heart-failure pathways.

Audience: cardiology trainees, imagers and inherited-cardiac-condition teams. Evidence reviewed: September 2026.

Key message

Arrhythmogenic cardiomyopathy (ACM) is a spectrum that may be right-dominant, biventricular or left-dominant. Imaging supports—but does not independently establish—the diagnosis. Electrical, structural, tissue, genetic and family data must be integrated.

When to suspect ACM

• Ventricular arrhythmia with morphology suggesting RV or LV origin.
• Unexplained regional ventricular dysfunction or aneurysm.
• Disproportionate RV dilatation or dysfunction.
• Subepicardial or ring-like non-ischaemic scar on CMR.
• A pathogenic variant or family history of ACM or premature sudden death.

Echocardiography

Perform a complete study with an RV-focused apical view. Assess RV dimensions, fractional area change, TAPSE, S′, free-wall strain and regional motion. Examine the RV outflow tract in parasternal long- and short-axis views. For the LV, quantify volumes and ejection fraction, examine regional deformation and look for subtle inferolateral dysfunction.

Regional akinesia, dyskinesia or aneurysm is more specific than subjective hypokinesia, but normal variants and poor windows are common. Prominent trabeculation or the moderator band is not diagnostic. Isolated mild RV enlargement in an athlete requires careful differentiation using proportional chamber remodelling, function, arrhythmia burden and tissue characterisation.

Cardiovascular magnetic resonance

CMR provides reproducible biventricular volumes and ejection fractions, regional cine assessment and myocardial tissue characterisation. Late gadolinium enhancement can identify non-ischaemic fibrosis; fat-sensitive observations alone are neither sufficiently specific nor central to modern diagnosis. Image quality, arrhythmia and partial-volume effects must be documented.

Criteria and differential diagnosis

The 2020 Padua criteria broadened assessment beyond classic right-dominant disease and incorporated CMR tissue criteria. The 2024 European Task Force criteria further address clinical diagnosis and phenotype. Apply the chosen framework explicitly and avoid mixing thresholds from different systems without explanation.

Important mimics include athlete’s heart, myocarditis, cardiac sarcoidosis, dilated cardiomyopathy, congenital shunts, pulmonary hypertension and idiopathic RV outflow-tract arrhythmia. Coronary disease should be considered for LV-predominant abnormalities.

Management implications

Management belongs in an inherited-cardiac-condition and electrophysiology pathway. It includes arrhythmic risk assessment, exercise counselling, family screening, genotype interpretation and consideration of an implantable cardioverter-defibrillator. Imaging severity alone should not determine sudden-death prevention.

Selected references

• International criteria for diagnosis of arrhythmogenic cardiomyopathy: the Padua criteria.
• 2024 European Task Force criteria for clinical diagnosis of arrhythmogenic cardiomyopathy.
• 2023 ESC cardiomyopathy guideline.

Educational material only. Suspected ACM requires specialist assessment, genetic counselling where appropriate and individualised arrhythmic-risk evaluation.

Audience: echocardiographers, cardiology trainees and valve teams. Evidence reviewed: September 2026.

Key message

Tricuspid stenosis is uncommon and usually coexists with regurgitation or left-sided valve disease. Diagnosis requires anatomy, haemodynamics and loading conditions to agree; a gradient alone is insufficient.

Anatomy first

The tricuspid apparatus comprises a large non-planar annulus, leaflets, chordae, papillary muscles, right ventricle and right atrium. Three-dimensional imaging often identifies anterior, posterior and septal leaflet segments more reliably than a single two-dimensional plane. Describe leaflet thickening, doming, restriction, commissural fusion, calcification, subvalvular involvement and device-lead interaction.

Causes

• Rheumatic disease, often with mitral involvement.
• Carcinoid heart disease.
• Congenital abnormality or prior repair.
• Endocarditis-related destruction or obstruction.
• Device leads, intracardiac masses and rare drug-related disease.

Echocardiographic approach

Acquire CW Doppler from the window with the most parallel inflow alignment, commonly apical or parasternal RV inflow. Use a slow sweep speed and measure at end-expiration when appropriate. Average at least three beats in sinus rhythm and more in atrial fibrillation. Report heart rate with the mean gradient. Valve area by pressure half-time is less robust for the tricuspid valve and is influenced by right-sided compliance and loading.

Severity and clinical integration

Severe disease is supported by clear anatomical restriction, persistently raised mean diastolic gradient at a stated heart rate, prolonged inflow, reduced valve area where measurement is credible, right-atrial enlargement and systemic venous congestion. Discordant data should trigger image review and, when necessary, transoesophageal echo, CT, CMR or invasive haemodynamics.

The 2025 ESC/EACTS guideline recommends intervention for symptomatic severe tricuspid stenosis and supports tricuspid surgery when severe stenosis is present during left-sided valve surgery. Decisions should be made by a multidisciplinary valve team, accounting for aetiology, regurgitation, RV function, pulmonary vascular disease and operative risk.

Reporting checklist

• Aetiology and leaflet/subvalvular morphology.
• Mean gradient, heart rate, rhythm and number of beats averaged.
• Degree and mechanism of associated TR.
• RA/RV remodelling, RV systolic function and estimated right-atrial pressure.
• Other valve lesions and evidence of systemic congestion.

Selected references

• 2025 ESC/EACTS valvular-heart-disease guideline.
• 2025 ESC/EACTS guideline—PubMed record.
• BSE guideline for tricuspid and pulmonary valve echocardiography.

Educational material only. Valve-intervention decisions require specialist multidisciplinary assessment.

Audience: echocardiographers and cardiology trainees. Evidence reviewed: September 2026.

Key message

Right-sided filling pressure cannot be read reliably from one Doppler waveform. Integrate inferior vena cava behaviour, tricuspid inflow, annular tissue Doppler, hepatic-vein flow, chamber morphology and the clinical setting.

Acquire physiology, not just traces

Record rhythm, heart rate, respiration and ventilation status. Tricuspid inflow is sampled at the leaflet tips in the apical four-chamber view. Tissue Doppler is obtained from the lateral tricuspid annulus. Hepatic-vein pulsed-wave Doppler is usually acquired from the subcostal window with a sample volume positioned within a hepatic vein, avoiding the vena caval junction.

How to interpret the components

Tricuspid E/A and deceleration time change with relaxation and pressure but have substantial overlap between normal and abnormal states. The E/e′ ratio on the right side has a weaker and more context-dependent relationship with right-atrial pressure than its familiar left-sided counterpart; it should not be used in isolation.

Normal hepatic-vein flow is generally systolic dominant. Reduced systolic predominance may accompany raised right-atrial pressure, but systolic flow reversal is particularly associated with severe tricuspid regurgitation. In atrial fibrillation, the atrial reversal wave disappears and beat selection becomes critical.

IVC diameter and inspiratory collapse provide a conventional estimate of right-atrial pressure in spontaneously breathing adults, but intermediate or discordant findings should prompt secondary signs rather than false precision. Mechanical ventilation invalidates simple application of spontaneous-breathing cut-offs.

Constrictive and restrictive physiology

Marked respiratory variation in atrioventricular inflow, hepatic-vein expiratory diastolic reversal, preserved or increased medial mitral e′ and septal shift can support constrictive physiology. No single sign is definitive. Technical quality, chronic obstructive pulmonary disease, volume status, rhythm and intrathoracic-pressure changes must be considered.

A practical synthesis

• First decide whether the signal is technically valid.
• Describe IVC findings and the assumptions used to estimate right-atrial pressure.
• Assess TR severity before interpreting hepatic-vein systolic reversal.
• Integrate RV size/function, septal configuration and pulmonary-pressure probability.
• State uncertainty when signals conflict or ventilation/rhythm limits interpretation.

Selected references

• ASE 2025 right-heart and pulmonary-hypertension guideline.
• BSE right-heart assessment guideline.
• 2022 ESC/ERS pulmonary-hypertension guideline.

Educational material only. Haemodynamic estimates require clinical correlation and invasive confirmation when management depends on precise pressure measurement.

Audience: echocardiographers and cardiology clinicians. Evidence reviewed: September 2026.

Key message

The right ventricle is geometrically complex and load dependent. Its assessment should integrate size, shape, regional motion, haemodynamic context and more than one systolic-function index.

Acquisition before measurement

Use a dedicated RV-focused apical four-chamber view rather than assuming the standard apical view is adequate. Rotate and tilt until the maximal RV long axis and cavity are displayed without foreshortening. Add parasternal long- and short-axis, RV inflow, subcostal and inferior vena cava views. Record end-expiratory images when respiration materially changes dimensions.

What to report

Core measurements

TAPSE measures longitudinal displacement of the lateral tricuspid annulus by M-mode. Tissue-Doppler S′ measures peak systolic annular velocity. FAC is calculated as (end-diastolic area − end-systolic area) / end-diastolic area × 100. Free-wall strain should exclude the septum when labelled “RV free-wall strain”; specify the convention because strain is normally reported as a negative percentage.

Thresholds are aids, not diagnoses. Current guidance should be checked for laboratory-, sex- and method-specific reference limits. Discordance is common: preserved TAPSE with reduced FAC or strain may reflect regional dysfunction, altered loading or postoperative mechanics.

Context changes interpretation

• Pressure overload: look for hypertrophy, septal flattening, reduced pulmonary acceleration time and pulmonary-hypertension signs.
• Volume overload: consider significant tricuspid or pulmonary regurgitation and shunts.
• Acute RV pressure load: chamber size and regional patterns may be more informative than wall thickness.
• Post-cardiotomy or transplant: longitudinal indices may fall despite preserved global output.
• Arrhythmia: average representative beats and state the rhythm.

Common failure modes

A single normal TAPSE does not exclude RV dysfunction. A visually “normal” RV should not replace measurements when clinical decisions depend on function. Severe tricuspid regurgitation can produce apparently vigorous annular movement despite impaired effective forward performance. Poor endocardial definition should be acknowledged rather than converted into a falsely precise FAC or strain value.

Suggested report language

“The right ventricle is [normal/mildly/moderately/severely dilated]. Global systolic function is [preserved/impaired], supported by TAPSE [x] mm, lateral S′ [x] cm/s, FAC [x]% and/or free-wall strain [x]%. Interpretation is made in the context of [loading condition/rhythm/image limitation].”

Selected references

• ASE 2025 right-heart and pulmonary-hypertension guideline.
• BSE practical guideline for right-heart assessment.
• ASE/EACVI chamber quantification.

Educational material only; individual findings require clinical integration and local reference ranges.

Audience: echocardiographers, cardiology trainees and clinicians interpreting cardiac ultrasound. Evidence reviewed: September 2026.

Key message

An echocardiographic image is a physical measurement, not a photograph. Diagnostic confidence depends on understanding how pulse frequency, propagation, beam geometry, signal processing and Doppler assumptions shape what appears on screen.

Learning objectives

• Relate frequency, wavelength and propagation speed to image quality.
• Distinguish axial, lateral and elevational resolution.
• Choose pulse-repetition frequency, scale, gain and filters intelligently.
• Recognise common artefacts before they become diagnostic errors.

How the pulse becomes an image

Piezoelectric elements convert electrical energy into ultrasound and returning mechanical energy into voltage. In soft tissue, scanners assume a propagation speed of approximately 1540 m/s. Depth is estimated from round-trip travel time. Because this speed is assumed rather than measured in each tissue, speed error can misplace structures.

Wavelength equals propagation speed divided by frequency. Higher-frequency imaging shortens wavelength and generally improves resolution, but attenuation rises and penetration falls. Adult transthoracic studies therefore require a compromise: use the highest frequency that still visualises the structure of interest.

Resolution is directional

Doppler: measure the component along the beam

The Doppler shift depends on transmitted frequency, blood velocity and the cosine of the insonation angle. Alignment matters: an angle error causes velocity underestimation and the error is amplified when velocity is squared in the simplified Bernoulli equation, ΔP = 4v².

Pulsed-wave Doppler provides range specificity but aliases when the Doppler shift exceeds the Nyquist limit, equal to half the pulse-repetition frequency. Continuous-wave Doppler measures high velocities without aliasing but cannot assign them to a unique depth. Colour Doppler displays mean velocity and variance within each sample region; it is a mapping tool, not a direct measure of regurgitant severity.

Controls that change the answer

• Overall gain and time-gain compensation: optimise signal without manufacturing tissue or erasing weak boundaries.
• Depth and sector width: keep only the anatomy needed to improve frame rate.
• Focus: place at or just below the structure of interest.
• Velocity scale and baseline: adjust to the expected flow; a low colour scale increases sensitivity but also blooming.
• Wall filter: suppresses low-frequency tissue motion but can remove genuine low-velocity flow.
• Dynamic range: changes contrast; excessive compression can conceal subtle boundaries.

Artefacts worth naming

Reverberation creates repeated interfaces; acoustic shadowing follows strongly attenuating structures; mirror artefact duplicates anatomy across a strong reflector; side lobes and grating lobes place off-axis reflectors in the main beam; refraction may duplicate or laterally displace anatomy. Confirm a suspected mass, defect or dissection plane in orthogonal views and with altered transducer position and settings.

A disciplined optimisation sequence

Begin with the clinical question. Select the window and frequency, minimise depth and sector width, position the focus, then adjust gain and compression. For Doppler, align the beam, choose the correct modality, optimise scale and sweep speed, and record several representative beats—more when rhythm or respiration varies. Measurements should follow current chamber and valve standards rather than a visually attractive but non-standard view.

Selected references

• ASE: comprehensive adult transthoracic echocardiography guideline.
• British Society of Echocardiography protocols and guidelines.
• ASE/EACVI chamber-quantification recommendations.

Educational material only. Apply local protocols, equipment-specific guidance and specialist review to individual patients.