Medical Licensing (MD/DO) · Independent exam preparation
European Exam in Core Cardiology: Clinical Reasoning Guide Study Guide
Practise imaging choices, valve intervention, arrhythmia treatment, coronary care and heart failure decisions through 60 focused concepts and original clinical drills.
By CertMedbry · Updated 20 October 2026
Practise choosing the next investigation, recognising haemodynamic danger, interpreting discordant measurements and selecting treatments that change outcomes. This selective guide gives equal attention to the four public EECC examination sections. The official UEMS examination blueprint defines the full scope, including topics beyond these 60 concepts; use it alongside current guidelines and wider cardiology reading.
Try 20 free practice questionsWhat is the exam format?
Check the question types, timing and outline before planning your revision.
Which examination and training level does this guide address?
This guide addresses the current European Exam in Core Cardiology, jointly organised by ESC, UEMS-CS and participating cardiac societies. It assesses the core knowledge cardiology specialty trainees need for independent practice. The January 2021 handbook explicitly identifies European Examination in General Cardiology, EEGC, as its former name; it does not establish the precise renaming date.
European Exam in Core Cardiology (EECC) · The European Examination in Core Cardiology — revised January 2021
How many questions are there, and how long is the examination?
The current examination page specifies 120 English clinical-scenario questions over three hours without a break. Each question has five options and one best answer. There is no negative marking. The page lists 16 June 2026 for the 2026 sitting; that date does not establish the date of a later examination.
Are scored questions, pretest questions and a fixed passing score identified?
The current public examination page does not specify a scored-versus-pretest allocation or a fixed passing percentage. Independent psychometric analysis and standard-setting review inform the final pass mark. Questions performing unexpectedly may be excluded after review. Historical handbook estimates should not be treated as a guaranteed current passing score.
How is the examination delivered, and is it adaptive?
The examination is delivered annually through CYIM/ProctorU online proctoring on the candidate's own computer, monitored by a human proctor. The supplied current page describes a 120-question paper and does not identify computer-adaptive testing. The UEMS selection page states that approximately 30% of questions include a still image or video clip.
European Exam in Core Cardiology (EECC) · Question Selection Group — UEMS Cardio
Which blueprint applies, and what changed with the 2026 curriculum?
The public UEMS blueprint available on 19 October 2026 maps 62 knowledge items from the 2020 ESC curriculum into four sections, each approximately 25% of the examination. It displays no revision or effective date. ESC published an updated training curriculum on 27 August 2026, but the current examination page and public blueprint still reference 2020. Adoption of replacement examination weights has not been established.
Question Selection Group — UEMS Cardio · European Exam in Core Cardiology (EECC) · Discover the ESC Core Curriculum for the Cardiologist · ESC Core Curriculum for the Cardiologist: 2026 update
Who determines eligibility, fees and the examination's national role?
Participating National or Affiliated Cardiac Societies determine eligibility, registration arrangements and trainee fees. Registration occurs through the society rather than individual entry. Societies determine how the examination fits their training programme and release results to candidates. Participation therefore does not establish a universal national licensing or exit-examination requirement.
European Exam in Core Cardiology (EECC) · European examination in core cardiology
How should these questions and flashcards be used?
The guide contains 15 concepts, five questions and five flashcards per public examination section. Its 20 original four-option questions are independent learning drills; the actual examination uses five options. They sample clinical reasoning and do not predict a pass. The ESC page identifies its registered-candidate preparatory course as the only official preparatory resource.
Question Selection Group — UEMS Cardio · European Exam in Core Cardiology (EECC)
The European Exam in Core Cardiology (EECC), formerly EEGC, assesses core knowledge for cardiology specialty training. It complements workplace assessment and does not independently establish overall specialist competence or medical licensure. This independent educational guide contains original learning material and is not an official ESC preparatory resource.
Outline used: Current public UEMS four-section examination blueprint, retrieved 2026-10-10; approximately 25% per section, based on the 2020 ESC Core Curriculum. The blueprint states no revision or effective date. The assigned EEGC label maps to the current European Exam in Core Cardiology (EECC): a historical handbook revised January 2021 explicitly identifies EEGC as its former name. The ESC training curriculum was updated on 27 August 2026, but the current examination page and public examination blueprint still explicitly reference the 2020 curriculum; adoption of a replacement examination blueprint was not established.
60 key concepts: understand, apply and avoid the traps
Work through the questions by exam domain. Explain the answer in your own words, try the example, then check the common pitfall.
Imaging and valvular heart diseaseapproximately 25%
1.How should echocardiography answer a valve question?
A useful echocardiographic assessment connects valve anatomy, lesion severity and the response of the chambers and pulmonary circulation. Transthoracic echocardiography usually establishes the initial haemodynamic picture. Transoesophageal imaging adds detail when acoustic windows are inadequate or a repair mechanism, prosthetic complication or endocarditis lesion needs clarification. Interpret Doppler findings with blood pressure, rhythm and flow: a technically precise velocity can still misrepresent severity when the physiological conditions are misunderstood.
Apply it
A patient has a loud murmur, exertional dyspnoea and poorly visualised mitral leaflets on transthoracic imaging. Define the regurgitant mechanism with transoesophageal imaging rather than making a repair decision from murmur intensity alone.
Common pitfall: A single colour jet image is tempting evidence of severity, but gain settings, eccentricity and loading conditions can change its apparent size substantially.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
2.When does CMR resolve an uncertain ventricular assessment?
Cardiac magnetic resonance provides reproducible ventricular volumes and function without relying on an acoustic window. It is particularly useful for right ventricular assessment and for quantifying regurgitation when echocardiographic findings conflict. Flow measurements and ventricular stroke volumes must be interpreted with associated shunts or additional regurgitant lesions. CMR complements echocardiography by answering a defined unresolved question; it does not replace urgent bedside assessment in an unstable patient.
Apply it
A repaired congenital heart disease patient has pulmonary regurgitation and a right ventricle that is difficult to measure by echocardiography. CMR can quantify right ventricular volumes and regurgitant flow to inform specialist review.
Common pitfall: Excellent ventricular measurements do not make CMR the automatic first investigation for shock. Bedside echocardiography usually supplies immediately actionable information much faster in that setting.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
3.Which questions favour coronary CT or functional imaging?
Coronary CT angiography describes coronary anatomy and is useful for excluding obstructive disease in appropriately selected patients. Functional imaging asks whether stress produces myocardial ischaemia, helping connect symptoms with physiological consequences. Heavy calcification, motion and an unsuitable rhythm can reduce CT interpretability. Stress echocardiography, perfusion CMR and nuclear perfusion imaging have different practical strengths. Select the test according to clinical likelihood, image quality, contraindications and the decision its result will change.
Apply it
A patient with stable exertional discomfort has extensive coronary calcification and a previous nondiagnostic CT study. A functional imaging strategy may better answer whether the symptoms correspond to inducible myocardial ischaemia.
Common pitfall: An anatomical narrowing does not automatically prove ischaemia, while a negative functional study does not establish absence of all coronary atherosclerosis or microvascular dysfunction.
2024 ESC Guidelines for the management of chronic coronary syndromes
4.What establishes high-gradient severe aortic stenosis?
Concordant severe aortic stenosis usually combines a peak aortic velocity of at least 4.0 m/s, mean gradient of at least 40 mmHg and valve area no greater than 1.0 cm². Symptoms attributable to the obstruction make intervention assessment urgent. Doppler alignment, left ventricular outflow tract measurements and flow conditions determine reliability. The valve area is calculated rather than directly measured, so an unexpectedly small area should prompt a technical and physiological review.
Apply it
A patient develops exertional syncope with a calcified aortic valve, peak velocity 4.5 m/s and mean gradient 48 mmHg. These concordant findings support symptomatic severe obstruction and prompt valve-team assessment.
Common pitfall: A preserved ejection fraction does not make severe symptomatic obstruction benign. Ejection fraction describes ventricular emptying and cannot exclude a dangerous fixed outflow obstruction.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
5.How is low-flow, low-gradient aortic stenosis clarified?
A small calculated valve area with a low gradient can reflect truly severe obstruction with insufficient forward flow or a valve that opens incompletely because ventricular contraction is weak. First check measurements, blood pressure and stroke volume. In reduced-ejection-fraction low-flow disease, low-dose dobutamine can distinguish persistent severe obstruction from increased opening as flow improves. CT valve-calcium assessment provides complementary evidence when stress findings are inconclusive or another low-gradient phenotype is present.
Apply it
A patient has valve area 0.8 cm², mean gradient 25 mmHg and ejection fraction 30%. During dobutamine, the gradient rises above 40 mmHg while valve area remains below 1.0 cm², supporting true severe stenosis.
Common pitfall: A low gradient alone does not exclude severe stenosis. Conversely, an isolated small calculated area should not trigger intervention before measurement error and flow are assessed.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
6.When does chronic aortic regurgitation threaten the ventricle?
Chronic aortic regurgitation causes left ventricular volume overload, initially compensated by chamber dilatation and increased total stroke volume. In asymptomatic severe regurgitation, surgery is recommended when LVEF is ≤50%, left ventricular end-systolic diameter (LVESD) is >50 mm, or indexed LVESD is >25 mm/m². These are alternative triggers; all three need not be present. Selected patients at low surgical risk may be considered for earlier intervention before these established thresholds, particularly when serial measurements show deteriorating ventricular function or progressive enlargement. Acute severe regurgitation can instead cause pulmonary oedema and circulatory collapse before ventricular dilatation develops.
Apply it
An asymptomatic patient with severe regurgitation and LVEF 45% meets a surgical trigger. Another patient with LVEF 55% and LVESD 52 mm also meets a trigger despite preserved reported exercise tolerance. Measure ventricular dimensions serially and index LVESD to body surface area, particularly in smaller adults.
Common pitfall: Do not wait for symptoms when a ventricular trigger is already present. Wide pulse pressure supports the clinical diagnosis but does not determine intervention timing, and its absence does not exclude acute severe regurgitation.
2025 ESC/EACTS valvular heart disease guidelines — official slide set · 2025-ESC-Guideline-Valvular-Heart-Disease.pdf
7.Why are ejection fraction and indexed ventricular size important in primary mitral regurgitation?
In primary mitral regurgitation, the ventricle ejects into both the aorta and the relatively low-pressure left atrium. Total LVEF can therefore appear preserved despite impaired myocardial performance. In asymptomatic severe primary regurgitation, LVEF ≤60%, left ventricular end-systolic diameter (LVESD) ≥40 mm, or indexed LVESD ≥20 mm/m² identifies ventricular dysfunction that triggers surgery. Each criterion can independently identify the threshold. Indexing prevents a smaller adult from being falsely reassured by an absolute LVESD below 40 mm. Durable valve repair is preferred when feasible.
Apply it
A patient with severe regurgitation from a flail posterior leaflet and LVEF 58% already meets a ventricular trigger despite reporting no limitation. A smaller patient with body surface area 1.6 m², LVESD 36 mm and LVEF 64% has indexed LVESD 22.5 mm/m² and also meets a trigger.
Common pitfall: An LVEF near 60% is not reassuring in severe primary mitral regurgitation. Likewise, checking only the absolute ventricular dimension can miss clinically significant enlargement in smaller adults. These thresholds concern severe primary disease and should not be transferred automatically to secondary mitral regurgitation.
2025 ESC/EACTS valvular heart disease guidelines — official slide set · 2025-ESC-Guideline-Valvular-Heart-Disease.pdf
8.How does secondary mitral regurgitation change the treatment sequence?
Secondary mitral regurgitation results from ventricular or atrial remodelling that disrupts leaflet coaptation despite the absence of a primary destructive leaflet lesion. Ventricular disease requires optimisation of heart failure treatment and resynchronisation when indicated before residual regurgitation is judged. Revascularisation may also matter when coronary disease contributes. Persistent severe symptomatic regurgitation can justify a valve intervention in selected patients, but anatomy, ventricular condition and expected benefit must be assessed together.
Apply it
A patient with a dilated ventricle, tethered mitral leaflets and severe regurgitation has received little heart failure treatment. Optimise myocardial therapy and assess device eligibility before deciding that a mitral procedure is the next step.
Common pitfall: A large jet does not establish a primary valve disorder. Treating the valve while leaving the underlying ventricular disease undertreated can miss the main mechanism.
2025 ESC/EACTS valvular heart disease guidelines — official slide set · 2026 ESC Guidelines for the management of heart failure — official slide set
9.Which mitral stenosis findings favour balloon commissurotomy?
Balloon mitral commissurotomy works by splitting fused commissures, making rheumatic commissural fusion the essential anatomical mechanism. Suitable symptomatic clinically significant stenosis requires favourable anatomy and assessment for left atrial thrombus and associated regurgitation. Left atrial thrombus or more than mild mitral regurgitation argues against the procedure. Degenerative annular calcification without commissural fusion is a different disease and does not provide the same target for balloon splitting.
Apply it
A symptomatic patient has rheumatic mitral stenosis, mobile leaflets and fused commissures. Transoesophageal imaging shows no left atrial thrombus and only mild regurgitation, supporting assessment for percutaneous commissurotomy at an experienced centre.
Common pitfall: Valve area alone does not establish procedural suitability. Balloon treatment of a heavily calcified valve without commissural fusion can fail or produce important regurgitation.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
10.How do tricuspid lesions produce systemic congestion?
Tricuspid regurgitation returns right ventricular systolic flow to the right atrium, producing venous congestion and progressive chamber dilatation. Functional disease commonly follows annular enlargement, atrial fibrillation, pulmonary hypertension or right ventricular remodelling. Tricuspid stenosis instead obstructs right atrial emptying during diastole and requires anatomical and Doppler confirmation. Assessment should integrate hepatic and renal consequences, right ventricular function and left-sided disease rather than treating peripheral oedema as a sufficient severity measure.
Apply it
A patient with longstanding atrial fibrillation has severe tricuspid regurgitation, a dilated annulus and hepatic congestion despite preserved left ventricular function. The mechanism may be atrial functional regurgitation rather than primary leaflet destruction.
Common pitfall: Diuresis can relieve oedema without correcting the valve lesion. Waiting for advanced right ventricular failure or organ dysfunction may reduce the benefit of intervention.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
11.What distinguishes pulmonary valve pressure and volume overload?
Pulmonary stenosis produces right ventricular pressure overload, favouring hypertrophy and a systolic outflow gradient. Pulmonary regurgitation produces volume overload, favouring progressive right ventricular dilatation and diastolic reverse flow. Echocardiography assesses valve anatomy, the location of obstruction, Doppler gradients and ventricular consequences. CMR quantifies pulmonary regurgitation and right ventricular volumes and systolic function, particularly when echocardiography incompletely characterises postoperative anatomy. Interpretation must incorporate the original congenital lesion and previous intervention. These assessments are addressed in the right ventricular outflow tract obstruction and tetralogy of Fallot sections of the [2020 ESC adult congenital heart disease guideline](https://academic.oup.com/eurheartj/article/42/6/563/5898606).
Apply it
An adult with repaired tetralogy of Fallot has substantial pulmonary regurgitation, increasing right ventricular size and only a small residual systolic outflow gradient. Use CMR to quantify regurgitant burden, right ventricular volumes and function. The dominant residual lesion may be regurgitation causing volume overload despite successful relief of the original obstruction.
Common pitfall: A low residual systolic gradient does not exclude important postoperative pulmonary valve disease. Assess obstruction and regurgitation separately: neither the gradient alone nor a qualitative description of the regurgitant jet establishes the full burden on the right ventricle.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
12.Why can one valve lesion distort another lesion's measurements?
Doppler gradients depend on flow as well as the severity of an obstruction. In multivalvular disease, one lesion can reduce forward stroke volume across another valve or increase the volume passing through it. A low gradient can consequently underestimate important stenosis, while high flow can exaggerate a gradient. Integrated assessment should identify the dominant mechanisms, quantify ventricular consequences and consider the combined haemodynamic burden rather than applying isolated-lesion thresholds without context.
Apply it
A patient has severe mitral regurgitation and a small aortic valve area but only a modest aortic gradient. Reduced forward aortic flow may explain the discrepancy and should be assessed before dismissing the stenosis.
Common pitfall: Adding two independently assigned severity labels does not describe their interaction. Flow redistribution can make measurements misleading even when each Doppler tracing is technically satisfactory.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
13.Which anticoagulant principle applies to mechanical valves?
Mechanical prosthetic valves require vitamin K antagonist anticoagulation because the prosthetic surface and altered flow create sustained thrombotic risk. Direct oral anticoagulants are not substitutes for this indication. The target INR depends on prosthesis characteristics, position and patient-related thromboembolic risk, so one target should not be applied indiscriminately. Anticoagulation review includes adherence, interactions, bleeding risk and procedural planning, with bridging decisions individualised to the valve and clinical situation.
Apply it
A patient with a mechanical mitral prosthesis requests a switch from warfarin to apixaban to avoid INR testing. Explain that vitamin K antagonist treatment remains necessary and address the practical barriers to monitoring.
Common pitfall: Evidence favouring direct oral anticoagulants in ordinary atrial fibrillation cannot be transferred to mechanical prostheses. The valve indication determines the required anticoagulant class.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
14.How is an unexpectedly high prosthetic valve gradient investigated?
A high prosthetic gradient can reflect obstruction, patient–prosthesis mismatch, increased flow or measurement error. Compare current findings with the postoperative baseline and assess leaflet motion, regurgitation and haemodynamic conditions. Thrombus, pannus and structural deterioration have different mechanisms and management implications. Transoesophageal echocardiography, CT or fluoroscopy can clarify the cause according to prosthesis type and the unresolved question. A new gradient increase is more concerning than an unchanged lifelong baseline.
Apply it
A patient with a mechanical valve develops dyspnoea after several weeks of subtherapeutic anticoagulation. The gradient has risen markedly from baseline, making prosthetic thrombosis an urgent possibility requiring dedicated assessment of leaflet motion.
Common pitfall: A high gradient is not synonymous with thrombosis. Treating presumed thrombus without assessing baseline haemodynamics and prosthesis motion can expose the patient to unnecessary risk.
2025 ESC/EACTS valvular heart disease guidelines — official slide set
15.When should negative echocardiography be challenged in endocarditis?
A negative initial echocardiogram does not exclude infective endocarditis when clinical probability remains high. Transoesophageal imaging is particularly important with prosthetic material, poor transthoracic views or concern for perivalvular complications. Repeat imaging after approximately five to seven days is appropriate when an initially normal or inconclusive examination conflicts with persistent suspicion. Cardiac CT and nuclear imaging can add evidence, especially in prosthetic-valve infection, but findings must be integrated with microbiology and clinical criteria.
Apply it
A patient with a prosthetic aortic valve has persistent typical-organism bacteraemia and an unrevealing transthoracic study. Proceed to transoesophageal imaging and consider complementary prosthetic-valve imaging rather than excluding infection from that first scan.
Common pitfall: Absence of a visible vegetation is not equivalent to absence of infection. Prosthetic shadowing and early disease can conceal lesions or important perivalvular extension.
2023 ESC endocarditis guidelines — SEC Spanish translation incorporating corrections
Rhythm disordersapproximately 25%
16.How does CHA2DS2-VA guide stroke prevention in atrial fibrillation?
The 2024 ESC approach uses CHA2DS2-VA without assigning a point for sex. Heart failure, hypertension, diabetes, vascular disease and age 65–74 years each contribute one point. Age ≥75 years contributes two points instead of the single age point. Previous stroke, transient ischaemic attack or arterial thromboembolism contributes two points; these events form one component rather than separate additive categories. Oral anticoagulation is recommended at a score ≥2 and should be considered at a score of 1. Bleeding assessment should identify modifiable hazards rather than automatically override stroke prevention.
Apply it
A 68-year-old patient with hypertension and atrial fibrillation scores two points: one for age and one for hypertension. Anticoagulation is recommended in the absence of a contraindication. If the same patient previously had a transient ischaemic attack, the score becomes four, even if the neurological symptoms resolved completely.
Common pitfall: A transient ischaemic attack counts despite leaving no persistent deficit. Mild palpitations, infrequent recognised episodes or successful rhythm control do not erase established clinical stroke-risk factors.
2024 ESC Guidelines for the management of atrial fibrillation
17.What anticoagulation is required before and after cardioversion?
For atrial fibrillation lasting >24 hours or of uncertain duration, scheduled cardioversion requires at least three weeks of therapeutic anticoagulation beforehand, or transoesophageal echocardiographic exclusion of atrial thrombus with periprocedural anticoagulation. A negative transoesophageal study does not remove the need for anticoagulation accompanying cardioversion. Continue therapeutic anticoagulation for at least four weeks afterward because atrial mechanical stunning can promote new thrombus despite restoration of sinus rhythm. Post-cardioversion anticoagulation is optional only in the narrow situation of definite onset within 24 hours and no thromboembolic risk factors. Determine longer-term anticoagulation separately from the patient's stroke risk.
Apply it
A stable, previously unanticoagulated patient has continuous AF for four days. Either anticoagulate therapeutically for at least three weeks before cardioversion or use transoesophageal imaging to exclude thrombus and provide periprocedural anticoagulation. Both pathways require at least four weeks of anticoagulation afterward.
Common pitfall: Do not equate electrical recovery with immediate atrial mechanical recovery. When AF causes haemodynamic instability, perform urgent electrical cardioversion and initiate anticoagulation as soon as possible without delaying stabilisation.
2024 ESC Guidelines for the management of atrial fibrillation
18.What does AF-CARE add beyond rate control?
AF-CARE links comorbidity and risk-factor management, avoidance of stroke, reduction of symptoms through rate or rhythm control, and evaluation with repeated reassessment. Hypertension, obesity, sleep-disordered breathing and other contributors can sustain the atrial substrate and undermine symptom treatment. Rate control reduces the ventricular response, whereas rhythm control aims to restore or maintain sinus rhythm. Neither approach replaces stroke prevention, and treatment should evolve as symptoms, ventricular function and patient priorities change.
Apply it
A patient remains symptomatic despite an acceptable resting rate and has obesity and poorly controlled hypertension. Discuss rhythm-control options while actively addressing those contributors and reassessing anticoagulation, rather than merely increasing the rate-slowing medication.
Common pitfall: Treating atrial fibrillation as an isolated ECG problem misses modifiable disease drivers. Good resting rate control does not prove satisfactory exercise control or symptom relief.
2024 ESC Guidelines for the management of atrial fibrillation — official overview · 2024 ESC Guidelines for the management of atrial fibrillation
19.When can anticoagulation stop after atrial fibrillation ablation?
Ablation reduces arrhythmia burden but does not erase the atrial disease or clinical factors responsible for embolic risk. Anticoagulation is continued for at least two months after the procedure, and longer-term treatment follows thromboembolic risk rather than apparent procedural success. Asymptomatic recurrences and incomplete monitoring make symptom-based decisions unreliable. A patient with an ongoing anticoagulation indication should therefore not stop treatment merely because follow-up recordings show sinus rhythm.
Apply it
A 77-year-old patient with hypertension has no detected atrial fibrillation six months after ablation. Age and hypertension still establish substantial thromboembolic risk, so the reassuring rhythm follow-up alone does not justify stopping anticoagulation.
Common pitfall: A successful rhythm procedure is not a validated substitute for risk-based stroke prevention. Absence of palpitations also fails to exclude recurrent silent atrial fibrillation.
2024 ESC Guidelines for the management of atrial fibrillation
20.Why is AV-nodal blockade dangerous in pre-excited atrial fibrillation?
In pre-excited atrial fibrillation, an accessory pathway can conduct rapid atrial impulses directly to the ventricles. Blocking the AV node can favour accessory-pathway conduction and precipitate ventricular fibrillation. An irregular, very rapid wide-complex rhythm with changing QRS appearance should raise this concern. Unstable patients need electrical cardioversion. In suitable stable patients, agents that act on the accessory pathway, such as procainamide or ibutilide, are options under appropriate monitored specialist care.
Apply it
A young patient with previous delta waves develops an irregular broad-complex tachycardia at approximately 240 beats per minute. Avoid diltiazem or adenosine; choose treatment for pre-excited atrial fibrillation according to haemodynamic stability.
Common pitfall: The usual narrow-complex atrial fibrillation rate-control algorithm is hazardous here. Intravenous amiodarone is also contraindicated in this setting under the cited atrial fibrillation guidance.
2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation
21.When is adenosine useful for regular narrow-complex tachycardia?
In a stable regular narrow-complex tachycardia, vagal manoeuvres and then adenosine can interrupt a circuit that depends on AV-nodal conduction, such as AV-nodal re-entry or orthodromic AV re-entry. Transient AV block can also reveal underlying atrial activity without terminating its source. Continuous rhythm recording helps distinguish termination from diagnostic unmasking. Confirm regularity and stability first, and recognise that an irregular wide-complex rhythm requires a different and potentially more urgent approach.
Apply it
A stable adult has abrupt-onset palpitations with a regular narrow-complex rate of 185. After an unsuccessful modified Valsalva manoeuvre, monitored adenosine is a reasonable next intervention while recording the rhythm response continuously.
Common pitfall: Failure to terminate does not make adenosine diagnostically useless. Brief AV block may uncover flutter waves and identify an atrial rhythm that continues independently.
22.How can atrial flutter hide behind a regular rate of 150?
Typical atrial flutter often has an atrial rate near 300 beats per minute. With 2:1 AV conduction, the ventricular rhythm can be strikingly regular near 150, and alternate flutter waves may be hidden within QRS complexes or T waves. Temporary AV-nodal slowing may expose continuing atrial activity. Diagnosis matters because flutter is an atrial macro-re-entrant rhythm, not simply a generic supraventricular tachycardia, and anticoagulation and rhythm-management decisions require appropriate assessment.
Apply it
A patient has persistent regular narrow-complex tachycardia at 150. Adenosine briefly slows ventricular conduction and reveals repetitive atrial waves, but the atrial rhythm continues. This response supports flutter rather than AV-nodal re-entrant tachycardia.
Common pitfall: A rate near 150 is a clue rather than a diagnostic criterion. Sinus tachycardia and other supraventricular rhythms remain possible without confirming atrial activity.
2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation · 2025 AHA Guidelines — Part 9: Adult Advanced Life Support
23.Which clues favour ventricular tachycardia in a broad-complex rhythm?
A regular broad-complex tachycardia in a patient with previous infarction or structural heart disease should be presumed ventricular until a safer alternative is established. AV dissociation, capture beats and fusion beats strongly support a ventricular origin. Preserved blood pressure does not distinguish ventricular tachycardia from supraventricular tachycardia with aberrancy. Management depends on stability and rhythm morphology, with continuous monitoring and readiness for electrical treatment rather than empiric application of a narrow-complex algorithm.
Apply it
A patient with an old anterior infarction has a regular broad-complex tachycardia at 170 and occasional normal-looking capture beats. The substrate and AV dissociation clues support ventricular tachycardia despite an initially adequate blood pressure.
Common pitfall: Haemodynamic tolerance does not prove a supraventricular mechanism. Some sustained ventricular tachycardias remain tolerated until deterioration occurs or an inappropriate drug worsens the situation.
24.How does QT duration distinguish torsades from other polymorphic VT?
Torsades de pointes is polymorphic ventricular tachycardia associated with prolonged repolarisation, often following a pause. QT-prolonging medicines, hypokalaemia, hypomagnesaemia and bradycardia can create the substrate. Recurrent episodes require removal of triggers, electrolyte correction and intravenous magnesium; selected pause-dependent cases need heart-rate acceleration. Polymorphic ventricular tachycardia with a normal preceding QT suggests a different mechanism, commonly acute ischaemia. Sustained polymorphic ventricular tachycardia requires immediate unsynchronised shock because reliable synchronisation is difficult.
Apply it
A patient taking a QT-prolonging antibiotic develops pause-triggered polymorphic tachycardia with QTc 580 ms and potassium 3.0 mmol/L. Correct the acquired long-QT substrate and use magnesium alongside immediate electrical treatment when the rhythm is sustained.
Common pitfall: Polymorphic appearance alone does not establish torsades. Giving a QT-prolonging antiarrhythmic to acquired long-QT torsades can worsen the mechanism responsible for recurrent episodes.
25.When should tachycardia receive immediate electrical treatment?
Tachycardia causing hypotension, shock, ongoing ischaemic discomfort, acute heart failure or altered mental status requires prompt electrical treatment. Regular monomorphic tachycardia and atrial fibrillation with a pulse generally receive synchronised cardioversion. Sustained polymorphic ventricular tachycardia requires an unsynchronised shock, while pulseless rhythms follow the cardiac-arrest algorithm. The causal link matters: sinus tachycardia compensating for haemorrhage should prompt treatment of bleeding rather than an attempt to cardiovert a physiological response.
Apply it
A patient develops regular monomorphic tachycardia with a pulse, blood pressure 70/40 and confusion. Perform synchronised cardioversion promptly, with sedation when feasible, rather than waiting for a prolonged sequence of diagnostic drug trials.
Common pitfall: An abnormal rate is not sufficient reason to shock. Determine whether the rhythm causes instability or reflects an underlying emergency requiring its own treatment.
26.Which AV blocks justify pacing without symptom correlation?
Acquired Mobitz II, high-grade AV block and complete AV block warrant permanent pacing when they are not attributable to a reversible or physiological cause, even without documented symptoms. Their risk differs from benign AV-nodal delay because conduction can fail unpredictably. Evaluate medication effects, metabolic abnormalities and relevant acute disease before assigning permanence. Temporary support may be necessary during instability, but a stable presentation does not remove the long-term pacing indication once irreversible advanced block is established.
Apply it
An older adult has persistent complete AV dissociation with a ventricular escape rate of 34. Electrolytes are normal and no reversible medication or acute cause is identified. Permanent pacing is indicated despite denial of syncope.
Common pitfall: Waiting for a blackout is unnecessary in irreversible advanced AV block. Symptom correlation is central to many sinus-node decisions but does not govern these indications.
Bradycardia and Cardiac Conduction Delay — Top Things to Know
27.Why does sinus-node dysfunction require symptom correlation?
Sinus-node dysfunction includes inappropriate sinus bradycardia, pauses and impaired heart-rate response to activity. There is no single minimum heart rate or pause duration that automatically establishes a permanent pacing indication. Documenting a temporal relationship between symptoms and bradycardia is therefore central, alongside assessment of reversible causes. Nocturnal bradycardia should prompt consideration of sleep-disordered breathing and does not itself establish a pacing indication. The objective is relief of attributable symptoms.
Apply it
A patient reports dizziness but an incidental overnight recording shows sinus rates of 38 without symptoms. Seek symptom–rhythm correlation and assess relevant contributors rather than recommending a pacemaker solely because of the recorded minimum rate.
Common pitfall: A striking monitor number can distract from causation. Bradycardia occurring during sleep may be unrelated to daytime dizziness and may not benefit from pacing.
Bradycardia and Cardiac Conduction Delay — Top Things to Know
28.How should monitoring match the frequency of palpitations or syncope?
Ambulatory monitoring is useful when its recording period has a realistic chance of capturing the suspected event. Daily symptoms may suit short continuous monitoring, whereas infrequent unexplained episodes require longer monitoring strategies. A symptom diary and event timing help establish causation. High-risk presentations, including exertional syncope, structural disease or suspected advanced conduction disease, need urgent assessment rather than routine outpatient reassurance. A negative recording without a representative event does not exclude an intermittent arrhythmia.
Apply it
A patient has unexplained loss of consciousness every two months and a normal 24-hour recording without symptoms. A longer monitoring strategy is more informative than repeatedly ordering short recordings that are unlikely to capture an event.
Common pitfall: A normal monitor is reassuring only for the period and events it sampled. Failure to record the patient's characteristic episode leaves the central diagnostic question unresolved.
Bradycardia and Cardiac Conduction Delay — Top Things to Know
29.When is an ICD indicated for primary prevention in ischaemic heart failure?
An implantable cardioverter defibrillator detects and treats life-threatening ventricular tachyarrhythmias. An established ischaemic primary-prevention indication is symptomatic NYHA II–III heart failure with LVEF ≤35% despite at least three months of optimal foundational therapy, no myocardial infarction within the preceding 40 days, and expected survival exceeding one year with good functional status. Foundational therapy includes an appropriate renin–angiotensin system inhibitor, an evidence-based beta-blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor, as tolerated. The waiting period allows ventricular recovery and avoids assuming that an early post-infarction low LVEF is permanent.
Apply it
Eight months after myocardial infarction, a patient remains NYHA II with LVEF 30% despite four months of optimal therapy and has otherwise good functional status and life expectancy. This supports primary-prevention ICD implantation. A survivor of haemodynamically unstable sustained ventricular tachycardia without a reversible cause instead requires secondary-prevention assessment.
Common pitfall: Do not apply the primary-prevention waiting rule indiscriminately to secondary prevention. Other cardiomyopathies have disease-specific risk pathways. An ICD treats arrhythmias; it does not reverse congestion, progressive pump failure or competing terminal illness.
2026 ESC Guidelines for the management of heart failure — official slide set
30.When does ventricular dyssynchrony justify cardiac resynchronisation therapy?
Repeated right ventricular pacing can cause asynchronous ventricular contraction, adverse remodelling and worsening systolic function. CRT upgrade should be considered in patients with LVEF ≤35%, worsening heart failure despite optimal medical therapy and substantial right ventricular pacing. This differs from the standard native-conduction indication: symptomatic heart failure with LVEF ≤35% despite optimal therapy, sinus rhythm, left bundle branch block and QRS duration ≥150 ms. In that setting, CRT is recommended to improve symptoms and reduce morbidity and mortality. A bundle-branch abnormality alone does not establish eligibility.
Apply it
A pacemaker recipient develops worsening heart failure, LVEF 30% despite optimal therapy and 95% right ventricular pacing. After assessing other causes of deterioration, these findings support considering CRT upgrade. Separately, a symptomatic patient in sinus rhythm with LVEF 30%, native LBBB and QRS 160 ms meets the standard conduction-based indication.
Common pitfall: Normal lead thresholds and battery function establish technical device performance, not physiological synchrony. Distinguish the native QRS pattern from the paced QRS and assess pacing burden, symptoms, ventricular function and medical treatment together.
2026 ESC Guidelines for the management of heart failure — official slide set · Bradycardia and Cardiac Conduction Delay — Top Things to Know
Coronary artery disease, acute cardiovascular care, rehabilitation and sports cardiologyapproximately 25%
31.When should STEMI reperfusion proceed before troponin results?
A compatible ischaemic presentation with diagnostic persistent ST elevation requires immediate activation of a reperfusion pathway; an initially normal troponin must not delay treatment. Under the [2023 ESC ACS guideline](https://academic.oup.com/eurheartj/article/44/38/3720/7243210), primary PCI is preferred when PCI-mediated reperfusion, defined by wire crossing of the infarct-related artery, can occur within 120 minutes of STEMI diagnosis. If this cannot be achieved, patients presenting within 12 hours of symptom onset should receive fibrinolysis when eligible, followed by immediate transfer to a PCI centre. Assess fibrinolysis contraindications and haemodynamic status while arranging reperfusion.
Apply it
A haemodynamically stable patient presents 40 minutes after chest-pain onset with diagnostic regional ST elevation and reciprocal changes. If anticipated diagnosis-to-wire-crossing time is 100 minutes, arrange primary PCI without waiting for troponin. In a contrasting case with the same presentation but an anticipated interval of 170 minutes, give fibrinolysis if there are no contraindications and transfer immediately to a PCI centre.
Common pitfall: The 120-minute interval starts at STEMI diagnosis and ends at PCI-mediated reperfusion. It is neither the ambulance journey alone nor the interval from symptom onset. Include dispatch, transfer and catheterisation preparation in the estimate. Symptom onset determines the separate 12-hour fibrinolysis eligibility window; waiting for repeat troponin can waste salvageable myocardium.
2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes
32.What separates myocardial injury from myocardial infarction?
An elevated cardiac troponin establishes myocardial injury, and a rise or fall supports an acute process. Myocardial infarction additionally requires evidence that the injury is ischaemic, such as compatible symptoms, ECG changes or new regional loss of viable myocardium. Sepsis, tachyarrhythmia and heart failure can elevate troponin through other mechanisms. Clinical context distinguishes an acute coronary plaque event from supply–demand imbalance or non-ischaemic injury and determines whether an acute coronary strategy is appropriate.
Apply it
A patient with severe pneumonia has a small dynamic troponin elevation but no ischaemic symptoms, ECG changes or new regional dysfunction. Investigate the injury in context rather than diagnosing a coronary plaque event from troponin alone.
Common pitfall: Troponin is highly specific for myocardial injury, not for its cause. Labelling every elevation as acute coronary thrombosis can lead to inappropriate treatment and missed alternatives.
2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes
33.Which ACS findings change oxygen and nitrate use?
In acute coronary syndrome, give supplemental oxygen when oxygen saturation is <90%; routine supplementation is not recommended at saturation ≥90%. Nitrates relieve ischaemic discomfort through vasodilatation but can dangerously reduce preload and blood pressure. Avoid them in hypotension or suspected right ventricular infarction. Also avoid nitrates within 12 hours of avanafil, 24 hours of sildenafil or vardenafil, and 48 hours of tadalafil. Nitrates increase cyclic GMP production, while phosphodiesterase-5 inhibitors prevent its breakdown; their combined vasodilator effect can cause profound hypotension.
Apply it
A patient with ACS has saturation 97%, blood pressure 88/60 mmHg and sildenafil use eight hours earlier. Routine oxygen is unnecessary, and nitrates are contraindicated by both hypotension and the drug interaction. Establish the exact agent and time taken rather than recording only unspecified recent use.
Common pitfall: The phosphodiesterase-5 inhibitor exclusion interval is agent-specific. Passing that interval does not make nitrates appropriate if hypotension or another contraindication persists. Oxygen and nitrate decisions do not replace urgent reperfusion and haemodynamic assessment.
2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes
34.Why does radial access matter during ACS intervention?
Radial arterial access reduces access-site bleeding and vascular complications compared with femoral access in appropriately performed acute coronary intervention, with associated clinical outcome benefits. Access choice remains sensitive to anatomy, procedural needs and operator expertise. Prevention of bleeding also requires attention to antithrombotic selection, renal function and subsequent monitoring. After any intervention, new hypotension, pain, limb ischaemia or falling haemoglobin should trigger assessment for procedural complications rather than being attributed automatically to the original coronary syndrome.
Apply it
An older patient with acute coronary syndrome and increased bleeding risk requires PCI. When technically suitable and supported by operator expertise, radial access is a useful component of the strategy to reduce bleeding complications.
Common pitfall: Radial access reduces an important source of bleeding but does not eliminate systemic haemorrhage. Post-procedure deterioration still requires review of haemoglobin, haemodynamics and other potential bleeding sites.
ACC, AHA Issue New Acute Coronary Syndromes Guideline · 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes
35.What should sudden shock after infarction make you suspect?
Post-infarction shock can result from extensive pump failure, recurrent ischaemia, arrhythmia or a mechanical complication. Abrupt pulmonary oedema with a new murmur raises concern for acute mitral regurgitation or septal rupture; sudden collapse can indicate free-wall rupture and tamponade. Urgent bedside echocardiography can distinguish mechanisms and direct immediate specialist treatment. A faint murmur does not exclude catastrophic regurgitation because rapid pressure equalisation can reduce its intensity during profound haemodynamic compromise.
Apply it
Several days after infarction, a patient suddenly develops pulmonary oedema and hypotension with a new systolic murmur. Obtain immediate bedside echocardiography and urgent mechanical-complication assessment rather than assuming gradual progression of uncomplicated left ventricular failure.
Common pitfall: The severity of a mechanical complication cannot be judged from murmur loudness. Rapid deterioration should outweigh a deceptively quiet examination in a shocked post-infarction patient.
2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes
36.Which actions take priority in ventricular fibrillation arrest?
Ventricular fibrillation is a shockable cardiac-arrest rhythm. Immediate high-quality CPR and prompt defibrillation are the central actions, with interruptions kept short and compressions resumed after shock delivery. Drugs and advanced airway procedures support the algorithm but should not delay its effective core. Reversible causes, including coronary thrombosis, hypoxia and electrolyte disorders, require parallel assessment. After return of circulation, structured stabilisation and investigation are needed rather than treating a palpable pulse as completion of care.
Apply it
A monitored patient collapses with ventricular fibrillation and no pulse while a defibrillator is available. Deliver prompt defibrillation within the resuscitation sequence and resume compressions rather than delaying for an advanced airway or blood sampling.
Common pitfall: An organised electrical rhythm after a shock does not guarantee circulation. Keep pulse checks brief and follow the arrest algorithm rather than pausing repeatedly for prolonged assessment.
37.How should stable chest-pain testing follow clinical likelihood?
Testing for chronic coronary disease begins with symptoms, risk factors, examination and an estimate of obstructive disease likelihood. A very low likelihood may make testing unnecessary, while an appropriate non-invasive test can clarify intermediate uncertainty. Coronary CT assesses anatomy; functional imaging assesses ischaemia. Severe symptoms, high-risk findings or substantial clinical concern can justify invasive assessment. The goal is to obtain information that changes management rather than ordering successive tests without a defined clinical decision.
Apply it
A patient has reproducible exertional pressure and several coronary risk factors but no acute instability. Choose an anatomical or functional investigation suited to clinical likelihood and patient characteristics rather than using a resting ECG to exclude coronary disease.
Common pitfall: A normal resting ECG does not rule out chronic coronary disease. Conversely, testing an extremely low-likelihood presentation can generate false positives and unnecessary downstream procedures.
2024 ESC Guidelines for the management of chronic coronary syndromes
38.When should coronary physiology guide an intermediate stenosis?
Angiographic percentage narrowing is an imperfect measure of a lesion's effect on myocardial blood flow. For an intermediate stenosis, pressure-derived physiology can determine haemodynamic significance: fractional flow reserve of 0.80 or lower and instantaneous wave-free ratio of 0.89 or lower are commonly used decision thresholds. Interpret measurements with technical quality and clinical context. Revascularisation decisions also consider symptoms, anatomy and prognosis; a visually impressive lesion is not automatically a physiologically important target.
Apply it
An elective angiogram shows a 60% coronary stenosis. A technically reliable FFR of 0.86 argues against that lesion causing significant flow limitation, supporting medical management rather than stenting solely because the narrowing looks substantial.
Common pitfall: An intermediate angiographic appearance cannot reliably settle physiological significance. Equally, pressure measurements must be technically sound before they are used to justify intervention or deferral.
2024 ESC Guidelines for the management of chronic coronary syndromes
39.Why can angina persist without obstructive coronary disease?
Myocardial ischaemia can arise from coronary microvascular dysfunction or epicardial vasospasm even when angiography shows no flow-limiting fixed stenosis. Impaired vasodilator reserve and abnormal vasoconstriction are distinct mechanisms that may coexist. Persistent symptoms therefore warrant a mechanism-based evaluation rather than dismissal after a non-obstructive angiogram. Selected functional testing can identify an endotype and guide treatment, while non-cardiac causes should still be considered through a careful assessment of the symptom pattern.
Apply it
A patient has recurrent angina and objective ischaemia despite non-obstructive coronary arteries. Consider microvascular dysfunction and vasospasm, with further functional assessment when appropriate, rather than telling the patient that normal large vessels exclude a coronary mechanism.
Common pitfall: A normal-looking angiogram assesses epicardial anatomy, not the full coronary circulation. It cannot by itself exclude abnormal microvascular resistance or transient coronary vasospasm.
2024 ESC Guidelines for the management of chronic coronary syndromes
40.What LDL-C goal applies to established coronary disease?
Established atherosclerotic coronary disease places a patient in a very-high-risk prevention category. The LDL-C goal combines an absolute concentration below 1.4 mmol/L, or 55 mg/dL, with at least a 50% reduction from baseline. The 2025 focused update retained these goals. Check adherence and response to maximally tolerated statin treatment, then add effective non-statin therapy as needed. Meeting only the percentage reduction or only the absolute concentration does not satisfy the combined target.
Apply it
A patient's LDL-C falls from 3.2 to 1.6 mmol/L after myocardial infarction. The reduction is 50%, but the absolute concentration remains above target, so review adherence and intensify lipid-lowering treatment as appropriate.
Common pitfall: A laboratory reference range is not a secondary-prevention target. A result labelled normal can still exceed the recommended LDL-C goal for established coronary disease.
2024 ESC Guidelines for the management of chronic coronary syndromes · 2025 Focused Update on Dyslipidaemias
41.How should blood pressure contribute to coronary prevention?
Blood pressure contributes continuously to vascular risk. For most treated patients with chronic coronary syndromes, the usual systolic target is 120–129 mmHg when tolerated. Assess control using repeated standardised measurements, supported by home or ambulatory monitoring when clinic readings are discordant. Confirmed above-target pressure should prompt assessment of adherence, lifestyle measures and medication intensification. Individualise treatment when symptomatic orthostatic hypotension or other intolerance prevents achieving the usual target; check standing pressure, renal function and treatment adverse effects rather than pursuing the numerical target regardless of symptoms.
Apply it
A patient with stable coronary disease has repeated clinic pressures around 148/84 mmHg and consistently elevated home readings despite taking prescribed treatment. With satisfactory standing pressure and no treatment intolerance, review adherence and intensify antihypertensive therapy toward a tolerated systolic pressure of 120–129 mmHg. Conversely, dizziness with substantially lower home and standing pressures warrants assessment before escalation.
Common pitfall: Neither a single high clinic reading nor a value below 140 mmHg proves that the treatment decision is correct. White-coat elevation can lead to overtreatment, while persistent systolic pressure of 136 mmHg remains above the usual treated target. Symptomatic orthostasis requires individualisation rather than automatic intensification.
2024 ESC Guidelines for the management of chronic coronary syndromes
42.Which diabetes treatments address cardiovascular risk beyond glucose?
In type 2 diabetes with established cardiovascular disease, glucose-lowering treatment should consider demonstrated cardiovascular and renal outcomes as well as glycated haemoglobin. Selected SGLT2 inhibitors and GLP-1 receptor agonists provide outcome benefits in relevant populations, with the preferred strategy influenced by heart failure, kidney disease, weight and individual contraindications. These choices complement lipid lowering, blood-pressure management, smoking cessation and antithrombotic decisions. A satisfactory glucose measurement does not remove the need for comprehensive vascular prevention.
Apply it
A patient with type 2 diabetes, previous infarction and heart failure has acceptable glycated haemoglobin on existing treatment. Review therapy for cardiovascular and renal benefit rather than assuming that the glucose result alone means treatment is complete.
Common pitfall: All glucose-lowering medicines are not interchangeable for cardiovascular outcomes. Selecting treatment solely by its glucose effect can overlook clinically important differences in heart failure and vascular benefit.
2024 ESC Guidelines for the management of chronic coronary syndromes
43.When is a primary-prevention risk score the wrong tool?
SCORE2 and SCORE2-OP support risk assessment in appropriate primary-prevention populations, incorporating age and relevant cardiovascular factors. They should not be used to downgrade the treatment needs of someone who already has established atherosclerotic disease. Such a patient belongs to secondary prevention, where the disease itself establishes substantial risk. Risk estimation also requires attention to populations for which separate approaches apply, including important diabetes, kidney disease and inherited lipid disorder contexts.
Apply it
A 56-year-old patient with a previous coronary stent asks whether a favourable calculated primary-prevention score means lipid therapy can stop. Explain that established coronary disease determines secondary-prevention management regardless of that calculation.
Common pitfall: A numerically low score can be misleading when applied outside its intended population. Always establish whether the patient already has cardiovascular disease before choosing a calculator.
What is new in the 2025 dyslipidaemia focused update · 2024 ESC Guidelines for the management of chronic coronary syndromes
44.What makes cardiac rehabilitation comprehensive?
Cardiac rehabilitation combines individually prescribed exercise with risk-factor treatment, education, medication support, nutritional care and psychosocial assessment. Depression, anxiety, social barriers and fear of exertion can undermine recovery even when the coronary procedure succeeds. Delivery should match clinical risk, patient needs and available support; selected patients can benefit from home-based or hybrid programmes. Rehabilitation therefore requires an assessment and progression plan rather than a generic instruction to walk more after discharge.
Apply it
After infarction, a patient avoids activity because of panic and cannot attend frequent hospital sessions. Assess exercise safety and psychological needs, then develop a supported rehabilitation plan that may include an appropriate home-based component.
Common pitfall: Exercise attendance alone does not prove comprehensive rehabilitation. Untreated depression, smoking, medication barriers or financial constraints can continue to drive risk and prevent sustained recovery.
2026 ESC Guidelines on Cardiac Rehabilitation — official slide set · Heart, body and mind — first ESC cardiac rehabilitation guidelines
45.How should exertional symptoms change exercise advice?
Exercise prescription should follow assessment of clinical stability, symptoms, functional capacity and the demands of the intended activity. New exertional chest discomfort, syncope or significant arrhythmia requires evaluation before vigorous training proceeds. A graded, individualised programme differs from unrestricted competitive exercise, where intensity and consequences of an event may be greater. Decisions should connect the underlying disease and objective exercise findings to a realistic activity plan rather than using age or apparent fitness as a clearance test.
Apply it
A recreational cyclist develops chest pressure during steep climbs after months without symptoms. Pause high-intensity efforts and assess possible ischaemia before prescribing a harder training programme simply because resting examination and daily walking remain comfortable.
Common pitfall: Good baseline fitness does not neutralise a new exertional warning symptom. A normal resting assessment may miss disease that becomes evident only under increased cardiovascular demand.
2026 ESC Guidelines on Cardiac Rehabilitation — official slide set · 2024 ESC Guidelines for the management of chronic coronary syndromes
Heart failure and cardiac patients in other settingsapproximately 25%
46.How is heart failure established beyond an ejection fraction?
Heart failure is a clinical syndrome requiring symptoms or signs linked to a structural or functional cardiac abnormality. Ejection fraction describes one aspect of ventricular performance but does not independently confirm or exclude the syndrome. Natriuretic peptides and imaging help establish cardiac dysfunction and raised filling pressures, interpreted with obesity, atrial fibrillation and kidney function. Preserved ventricular emptying can coexist with abnormal relaxation, stiffness and pulmonary congestion, so the diagnostic task is to explain the symptoms physiologically.
Apply it
A patient with breathlessness, oedema and preserved ejection fraction has left atrial enlargement and evidence of raised filling pressures. Evaluate a heart failure syndrome rather than excluding cardiac disease because ventricular emptying appears preserved.
Common pitfall: An ejection fraction alone is neither a diagnosis nor a complete haemodynamic assessment. Conversely, breathlessness with a normal ejection fraction should not automatically be labelled heart failure.
2026 ESC Guidelines for the management of heart failure — official slide set
47.Which therapies change outcomes in reduced systolic function?
Disease-modifying treatment for appropriate patients with reduced systolic function combines renin–angiotensin system inhibition, preferably an angiotensin receptor–neprilysin inhibitor when indicated, an evidence-based beta-blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor. These classes target complementary pathways and should be introduced and adjusted with attention to stability, blood pressure, potassium and renal function. Loop diuretics relieve fluid retention but do not substitute for the outcome benefits of the foundational treatment classes.
Apply it
A stable patient with ejection fraction 28% takes only furosemide and feels less breathless after diuresis. Review eligibility for complementary disease-modifying therapies rather than equating relief of oedema with adequate long-term treatment.
Common pitfall: Improved symptoms after diuresis can conceal persistent disease risk. Treatment review should distinguish congestion relief from medicines that reduce hospitalisation and mortality in appropriate patients.
2026 ESC Guidelines for the management of heart failure — official slide set
48.How do congestion and perfusion guide acute heart failure care?
Acute heart failure assessment separates fluid congestion from inadequate organ perfusion. Pulmonary or systemic congestion supports decongestive treatment, while cold extremities, confusion, oliguria and hypotension suggest threatened perfusion and a need for urgent haemodynamic assessment. These patterns can coexist. Identify triggers such as acute coronary disease, infection, arrhythmia or valve failure while monitoring response to therapy. Escalating diuretics alone is insufficient when shock or a correctable mechanical cause dominates the presentation.
Apply it
A patient has pulmonary oedema, cool limbs, confusion and low blood pressure. Treat this as congestion with possible hypoperfusion, urgently seeking the precipitating mechanism and appropriate monitored support rather than following a routine outpatient diuretic adjustment.
Common pitfall: Oedema does not establish adequate circulating perfusion. A congested patient can simultaneously be in shock, and reflex vasodilator treatment may worsen an already low pressure.
2026 ESC Guidelines for the management of heart failure — official slide set
49.When should improvement prompt advanced heart failure review?
Advanced heart failure referral should be considered before irreversible organ dysfunction develops. Recurrent admissions, persistent severe limitation, escalating diuretic needs, low blood pressure, worsening renal function or inability to tolerate disease-modifying therapy can signal a narrowing treatment window. A short-lived improvement after intravenous diuresis does not remove the underlying trajectory. Specialist review can assess advanced therapies, optimise conventional care and integrate symptom control and goals-of-care discussions according to clinical suitability and patient preference.
Apply it
A patient returns for a third decompensation in six months and now cannot tolerate previously effective medicines because of hypotension. Arrange advanced heart failure assessment despite improvement in ankle swelling during the current admission.
Common pitfall: Waiting until every treatment has become impossible can make referral too late. Repeated temporary rescue should trigger recognition of disease progression rather than repeated reassurance.
2026 ESC Guidelines for the management of heart failure — official slide set
50.Which tests distinguish ATTR from light-chain cardiac amyloidosis?
A non-biopsy diagnosis of transthyretin cardiac amyloidosis requires compatible echocardiographic or CMR findings, grade 2 or 3 myocardial uptake with an appropriate bone tracer such as 99mTc-PYP, DPD or HMDP, and exclusion of a monoclonal disorder. SPECT must confirm that uptake is myocardial rather than blood-pool activity. Grade 2 uptake equals bone uptake; grade 3 exceeds bone uptake. Monoclonal screening requires all three tests: serum free light chains, serum immunofixation and urine immunofixation. These criteria are set out in the [ESC cardiac amyloidosis position statement](https://academic.oup.com/eurjhf/article/23/4/512/8377837).
Apply it
A patient with otherwise unexplained ventricular wall thickening and compatible CMR findings has grade 3 uptake confirmed within myocardium by SPECT. If all three monoclonal screening tests exclude a monoclonal disorder, the findings establish ATTR cardiac amyloidosis without biopsy. If urine immunofixation instead detects a monoclonal protein, arrange urgent haematological assessment and tissue confirmation with amyloid typing: AL amyloidosis, ATTR with an incidental monoclonal gammopathy, or coexistence must be distinguished.
Common pitfall: Grade 1 myocardial uptake, which is less intense than bone uptake, does not establish a non-biopsy ATTR diagnosis and requires histological confirmation when amyloidosis remains suspected. Apparent uptake on planar imaging may represent blood pool, making SPECT essential. A monoclonal finding prevents attribution to ATTR from scintigraphy alone; it does not itself prove AL amyloidosis.
2026 ESC Guidelines for the management of heart failure — official slide set
51.When does suspected myocarditis require urgent escalation?
Myocarditis can present with chest pain, heart failure, conduction disease or ventricular arrhythmia. CMR can identify myocardial oedema and a non-ischaemic injury pattern, but haemodynamic instability, sustained ventricular arrhythmia or advanced AV block identifies a high-risk presentation needing urgent specialist assessment. Selected patients require endomyocardial biopsy when defining the cause will change treatment. A preceding viral illness is a contextual clue, not proof of a benign course or a specific aetiology.
Apply it
A patient develops chest pain after a respiratory illness and then has sustained ventricular tachycardia with deteriorating ventricular function. Escalate urgently rather than treating the history as uncomplicated post-viral discomfort suitable for routine outpatient follow-up.
Common pitfall: A young age and recent viral symptoms do not establish low risk. Electrical instability or shock outweighs reassuring demographics and demands a more urgent pathway.
2025 ESC myocarditis and pericarditis guidelines — official slide set
52.Why can a small pericardial effusion cause tamponade?
Tamponade occurs when pericardial pressure impairs cardiac filling, so the rate of fluid accumulation and pericardial compliance matter more than volume alone. Rapid bleeding can cause collapse with a relatively small effusion, whereas slowly accumulating fluid may become large before compromise occurs. Clinical shock and echocardiographic chamber-collapse findings require integrated interpretation. Unstable tamponade needs urgent drainage through the appropriate percutaneous or surgical route, with the suspected cause influencing the safest definitive approach.
Apply it
After a cardiac procedure, a patient develops hypotension and a new pericardial effusion with right-sided chamber collapse. Rapid accumulation can explain severe compromise even though the measured effusion is not exceptionally large on imaging.
Common pitfall: Effusion size is not a reliable stand-alone urgency scale. Waiting for a large fluid collection can be dangerous when rapidly rising pericardial pressure already limits filling.
2025 ESC myocarditis and pericarditis guidelines — official slide set
53.What explains persistent high venous pressure after effusion drainage?
Effusive-constrictive pericarditis combines an effusion with persistent constrictive restraint, usually involving the visceral pericardium. Removing fluid relieves the effusive component but does not necessarily normalise right atrial pressure or ventricular filling. Persistent venous congestion after adequate drainage should therefore prompt assessment for constriction as well as other causes of right-heart dysfunction. Doppler imaging, cross-sectional imaging and selected invasive haemodynamics can clarify the remaining physiological limitation and guide further treatment.
Apply it
A patient undergoes effective drainage of a significant effusion, yet jugular venous pressure remains high and filling abnormalities persist. Investigate effusive-constrictive physiology rather than assuming that all ongoing congestion means the drain has failed.
Common pitfall: Successful fluid removal does not prove normal pericardial mechanics. Persistent congestion can reflect residual constrictive restraint rather than immediate reaccumulation of a large effusion.
2025 ESC myocarditis and pericarditis guidelines — official slide set
54.How is pre-capillary pulmonary hypertension defined?
Pulmonary hypertension is defined haemodynamically by mean pulmonary arterial pressure above 20 mmHg at rest. A pre-capillary pattern additionally requires pulmonary arterial wedge pressure no greater than 15 mmHg and pulmonary vascular resistance above 2 Wood units. Right-heart catheterisation establishes these measurements; echocardiography estimates probability rather than definitively classifying haemodynamics. Distinguishing pre-capillary from post-capillary disease is essential because elevated pressure from left-heart filling abnormalities does not automatically represent pulmonary arterial hypertension.
Apply it
Right-heart catheterisation shows mean pulmonary arterial pressure 32 mmHg, wedge pressure 11 mmHg and cardiac output 4 L/min. Calculated resistance is 5.25 Wood units, establishing a pre-capillary haemodynamic pattern requiring classification of its cause.
Common pitfall: An elevated estimated pulmonary pressure on echocardiography does not establish pulmonary arterial hypertension. The wedge pressure, resistance and underlying disease determine the haemodynamic group.
2022 ESC/ERS pulmonary hypertension guidelines — SEC Spanish translation
55.Which test screens for chronic thromboembolic pulmonary hypertension?
Ventilation–perfusion lung scanning is recommended when evaluating suspected or newly diagnosed pulmonary hypertension to detect chronic thromboembolic disease. A normal perfusion study makes chronic thromboembolic pulmonary hypertension very unlikely in the appropriate setting, whereas mismatched defects require further assessment. CT provides important anatomical information but a previous CT report excluding acute embolism does not necessarily exclude chronic distal disease. Confirmed chronic thromboembolic disease warrants specialist assessment because treatment options depend on anatomy and haemodynamics.
Apply it
A patient remains breathless months after pulmonary embolism and now has echocardiographic evidence suggesting pulmonary hypertension. Obtain a ventilation–perfusion scan to assess chronic thromboembolic obstruction, even if an earlier CT excluded a new acute embolus.
Common pitfall: A history without recognised acute embolism does not exclude chronic thromboembolic disease. Conversely, persistent breathlessness after embolism is not automatically caused by recurrent acute thrombosis.
2022 ESC/ERS pulmonary hypertension guidelines — SEC Spanish translation
56.Why is the failing right ventricle sensitive to loading conditions?
The right ventricle is vulnerable to abrupt increases in pulmonary vascular load and depends on an effective balance between venous return, contractility and coronary perfusion. Excessive volume can worsen dilatation, tricuspid regurgitation and ventricular interaction, while inadequate filling can reduce output. Assessment therefore combines congestion, perfusion, pulmonary pressure and the underlying cause. Right-heart failure from pulmonary vascular disease requires specialist management rather than indiscriminate fluid loading or transfer of every left-heart treatment assumption.
Apply it
A patient with severe pulmonary hypertension has oedema, a markedly dilated right ventricle and low output. Assess venous congestion and perfusion carefully before giving large fluid boluses merely because systemic blood pressure is low.
Common pitfall: Low blood pressure does not prove volume depletion. In a distended failing right ventricle, additional fluid can worsen septal interaction and reduce effective left ventricular filling.
2022 ESC/ERS pulmonary hypertension guidelines — SEC Spanish translation
57.When can closing a congenital shunt be harmful?
A congenital systemic-to-pulmonary shunt can progressively damage the pulmonary vasculature. Once severe pulmonary vascular disease develops, bidirectional or right-to-left flow may cause cyanosis and the communication can serve as a pressure-relief pathway. Closing it without appropriate haemodynamic assessment can precipitate right-heart failure. Decisions require congenital and pulmonary hypertension expertise, including pulmonary vascular resistance and shunt direction. The mere presence of an anatomical defect does not establish that closure remains beneficial.
Apply it
An adult with an unrepaired septal defect has cyanosis, clubbing and severe pulmonary hypertension. Arrange specialist haemodynamic assessment rather than recommending closure on the assumption that every persistent communication should be eliminated.
Common pitfall: An anatomical repair can worsen physiology when advanced pulmonary vascular disease is established. Cyanosis and reversed shunting should challenge a straightforward defect-closure plan.
2022 ESC/ERS pulmonary hypertension guidelines — SEC Spanish translation
58.Why does pulmonary arterial hypertension make pregnancy high risk?
Pregnancy increases circulatory demand, but pulmonary arterial hypertension limits the ability of the pulmonary circulation to accommodate increased flow. The pressure-loaded right ventricle can therefore fail, particularly during the haemodynamic changes surrounding delivery and the postpartum period. Counselling must address serious maternal risk and pregnancy options through a specialist multidisciplinary team. The ESC/ERS guideline recommends stopping endothelin-receptor antagonists, riociguat and selexipag because of potential or unknown teratogenicity. This requires urgent specialist-directed treatment adjustment to protect maternal haemodynamics while addressing fetal medication hazards.
Apply it
A patient taking an endothelin-receptor antagonist reports a new pregnancy despite only mild symptoms. Arrange urgent pulmonary hypertension and pregnancy-team assessment, including discontinuation of the unsuitable drug and adjustment of the remaining regimen. Evaluate right ventricular function and clinical risk while discussing pregnancy options; do not wait for severe breathlessness.
Common pitfall: The recommendation to stop endothelin-receptor antagonists, riociguat and selexipag does not justify indiscriminate withdrawal of all pulmonary hypertension treatment. Maternal pulmonary vascular disease still requires active management. Apparent stability early in pregnancy neither establishes medication safety nor excludes subsequent right ventricular decompensation.
2022 ESC/ERS pulmonary hypertension guidelines — SEC Spanish translation
59.How is cancer therapy-related cardiac dysfunction defined and managed?
Moderate asymptomatic cancer therapy-related cardiac dysfunction includes a new LVEF reduction of ≥10 percentage points to 40–49%. A smaller reduction into that range requires an accompanying relative global longitudinal strain decline >15% from baseline or a new cardiac biomarker rise. Symptoms require separate assessment for a clinical heart failure syndrome. Management depends on the anticancer agent and severity: moderate asymptomatic dysfunction during anthracycline treatment generally warrants temporary interruption and heart failure therapy, whereas HER2-targeted therapy can generally continue with ACE inhibitor or ARB and beta-blocker treatment plus frequent surveillance. These distinctions follow the [2022 ESC cardio-oncology guideline](https://academic.oup.com/ehjcimaging/article/23/10/e333/6675075).
Apply it
An asymptomatic fall from LVEF 62% to 48% meets moderate dysfunction criteria. A fall from 52% to 46% requires additional strain or biomarker evidence to meet that definition. Confirm measurement quality, investigate alternative causes and identify the anticancer agent before choosing continuation or interruption.
Common pitfall: A ten-percentage-point decrease is an absolute change, not a 10% relative reduction. Do not apply one universal cancer-treatment interruption rule: anthracycline dysfunction, HER2-related dysfunction and suspected immune checkpoint inhibitor myocarditis require different decisions.
2026 ESC Guidelines for the management of heart failure — official slide set
60.When does the cause of haemopericardium change drainage strategy?
Blood in the pericardial space may follow instrumentation, trauma, myocardial rupture or an acute aortic catastrophe. Although tamponade physiology requires urgent action, definitive management depends on the source and whether bleeding continues. Suspected structural rupture can require immediate surgery rather than routine isolated pericardiocentesis. Bedside imaging should therefore be interpreted with the event history and examination, while resuscitation and surgical coordination proceed. Treating the pressure effect alone may leave the lethal bleeding mechanism unresolved.
Apply it
A patient with abrupt chest and back pain, shock and a new pericardial effusion may have an aortic source of haemopericardium. Seek immediate aortic and surgical assessment rather than treating the effusion as an isolated inflammatory problem.
Common pitfall: The same tamponade physiology can arise from very different diseases. Routine drainage without recognising active structural bleeding can fail to provide definitive control of the emergency.
2025 ESC myocarditis and pericarditis guidelines — official slide set
What to focus on during revision
The following are CertMedbry study suggestions. Use the official outline to check the full scope of your examination.
- Allocate approximately equal study time to the four public examination sections; equal section weighting does not imply that every individual topic appears annually.
- Build imaging reasoning around the unresolved question: anatomy, haemodynamics, tissue characterisation, ischaemia or procedural planning.
- Practise discordant valve measurements, regurgitant ventricular thresholds and prosthetic-valve complications alongside straightforward lesion recognition.
- Separate rhythm diagnosis, haemodynamic stabilisation, stroke prevention and device indications instead of treating them as one decision.
- Distinguish acute coronary occlusion from myocardial injury, anatomical stenosis from physiological significance, and symptom relief from outcome-changing prevention.
- Practise heart failure mechanisms, pulmonary haemodynamics, pericardial emergencies and specialist consultation triggers across different clinical settings.
- Use the full official outline to extend study into additional topics, including cardiac tumours, peripheral vascular disease, postoperative care and the wider congenital and pregnancy curriculum.
A practical preparation plan
1. Map the full examination scope
Start with the current public UEMS four-section blueprint and mark each knowledge item as secure, developing or unfamiliar. Use these 60 concepts as a selective starting set, then schedule additional reading for uncovered items.
2. Create decision-based notes
For each topic, record the decisive finding, the mechanism it supports, the next action and the main exception. Prioritise thresholds and contraindications that separate plausible management choices.
3. Integrate images and measurements
Practise ECGs, Doppler tracings, ventricular measurements, CT anatomy and haemodynamic calculations. State what each image or measurement establishes and what it cannot establish by itself.
4. Complete the balanced question set
Answer the 20 questions before reading the explanations. Review every alternative, identify the decisive cue and classify errors as knowledge gaps, misread physiology or unsafe prioritisation.
5. Use spaced clinical recall
Revisit the flashcards at increasing intervals. Expand each response with a brief contrasting case, such as complete AV block versus sinus-node dysfunction or true severe versus pseudo-severe aortic stenosis.
6. Rehearse sustained examination work
Build towards sustained mixed-topic practice reflecting the verified three-hour format. Use broader question resources for endurance; repeated performance on this small learning set is not an estimate of examination readiness.
Use your sample score as a starting point
The free set contains 20 original practice questions. It is a small learning sample, not an official examination or a validated pass prediction. Review each explanation and its source before moving to another topic.
Start the free sampleOfficial sources and updates
- European Exam in Core Cardiology (EECC)
- Question Selection Group — UEMS Cardio
- The European Examination in Core Cardiology — revised January 2021
- European examination in core cardiology
- Discover the ESC Core Curriculum for the Cardiologist
- ESC Core Curriculum for the Cardiologist: 2026 update
- 2025 ESC/EACTS valvular heart disease guidelines — official slide set
- 2023 ESC endocarditis guidelines — SEC Spanish translation incorporating corrections
- 2024 ESC Guidelines for the management of chronic coronary syndromes
- 2024 ESC Guidelines for the management of atrial fibrillation
- 2024 ESC Guidelines for the management of atrial fibrillation — official overview
- 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation
- Bradycardia and Cardiac Conduction Delay — Top Things to Know
- 2025 AHA Guidelines — Part 9: Adult Advanced Life Support
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- %CE%91%CE%BD%CF%84%CE%B9%CE%BC%CE%B5%CF%84%CF%8E%CF%80%CE%B9%CF%83%CE%B7-%CE%91%CF%83%CE%B8%CE%B5%CE%BD%CF%8E%CE%BD-%CE%BC%CE%B5-%CE%9F%CE%BE%CF%8D-%CE%A3%CF%84%CE%B5%CF%86%CE%B1%CE%BD%CE%B9%CE%B1%CE%AF%CE%BF-%CE%A3%CF%8D%CE%BD%CE%B4%CF%81%CE%BF%CE%BC%CE%BF-2025.pdf
- ehad191.pdf
- vrodeny_chyby_srdca_v_dospelosti_2020_guidelines.pdf
- kardio-onkologia_2022_guidelines.pdf
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