FCPS Cardiology TOACS - ECG, Echocardiography, Cath, CMR, CT, CXR, EP Tracings, Nuclear Scans

Attempt this exam to know your Score to get an idea of your fcps part 2 toacs preparation:

Welcome to cardiology toacs mock exam , there will be 40 stations, time for each station is usually 3 mins in the exam but in this video it will be, 1 min. you can pause the video if you need more time.

 Answer key is also shown in the video after 40 stations.

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In this comprehensive TOACS (Task Oriented Assessment of Clinical Skills) session, the candidate is taken through multiple diagnostic modalities in cardiology: surface ECG, chest-X-ray (CXR), echocardiography (Echo), cardiac catheterisation/angiography (Cath), cardiac CT, cardiac MRI (CMR), electrophysiology (EP) tracings, and nuclear scans (e.g., SPECT stress test). The aim is to test the ability of the trainee to interpret images/recordings, link them to the clinical scenario, derive diagnoses, and suggest appropriate next steps (management/investigations). The video shows multiple “stations” where you are given data (an ECG, a CXR, a CTA, etc), asked questions like “What is the abnormality?”, “What is the likely diagnosis?”, “What is the next best step?”, and “What is the management plan?”. The modalities emphasised include:

ECG: rhythm abnormalities, ST-T changes, conduction defects, hypertrophy patterns

CXR: cardiomegaly, pulmonary congestion, vascular redistribution, pleural effusions

Echocardiography: chamber sizes, valve lesions, ejection fraction, pericardial effusion, Doppler flows

Cardiac Cath / Angiography: coronary anatomy, lesions, intervention options

Cardiac CT / CMR: structural anomalies, functional assessment, tissue characterisation

EP tracings: arrhythmia mechanism, accessory pathways, ablation strategy

Nuclear scans / Stress imaging: perfusion defects, viability, ischaemia vs scar

The video emphasises integrating all this into one coherent clinical picture — not just recognising the finding, but relating it to the patient’s symptoms, risk factors, and what the next appropriate step is (for example, “If you see a large fixed perfusion defect on SPECT stress scan, then viability is low and CABG may not help; consider medical therapy,” or “If the CMR shows late gadolinium enhancement in a non-ischaemic pattern, suspect myocarditis or cardiomyopathy”).

The video thus serves as a mock assessment for the TOACS format job: you have to be quick, accurate, confident in interpretation, and ready to justify reasoning. For exam preparation it’s excellent because it covers exactly the kinds of stations you will face, emphasising pattern recognition + decision making.

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Commonly Asked Questions for FCPS Cardiology TOACS & Sample Answers

Here are some frequently asked types of questions with model answers you can use in your blog.

Q1. On ECG you see broad QRS with delta wave and short PR — what is the diagnosis? What is the next step?

Answer: The ECG features (short PR interval, delta wave, wide QRS) point to pre-excitation via an accessory pathway, consistent with Wolff‑Parkinson‑White syndrome. The next step is to assess symptoms (syncope, palpitations), look for arrhythmia history (AVRT, atrial fibrillation). In a symptomatic patient or high-risk pathway, refer for EP study and consider catheter ablation. In asymptomatic low-risk patients, manage conservatively but counsel about signs of life-threatening arrhythmia.

Q2. You are shown a CXR with enlarged cardiac silhouette, pulmonary venous congestion and pleural effusion in a patient with dyspnoea. Which diagnosis and what investigation next?

Answer: The radiographic appearance suggests left ventricular failure leading to cardiomegaly, pulmonary venous hypertension and pleural effusion. In the context of dyspnoea, one should suspect chronic heart failure (e.g., dilated cardiomyopathy) or acute decompensation. The next investigation is echocardiography to assess LV size, function (ejection fraction), valve lesions, and to look for pericardial effusion or other structural causes. Additionally, check BNP/NT-proBNP, renal function and rule out acute coronary syndrome.

Q3. On Echo you see severe mitral regurgitation with flail leaflet, left atrial enlargement and normal LV size. What is the likely cause and management?

Answer: A flail mitral leaflet with severe MR and left atrial enlargement but relatively preserved LV size suggests primary (degenerative) mitral valve disease (e.g., chordal rupture) rather than secondary (ventricular) MR. The likely cause is myxomatous degeneration leading to leaflet rupture. Management: symptomatic severe MR or evidence of LV dysfunction/enlargement or pulmonary hypertension warrants referral for mitral valve repair (if feasible) rather than replacement, ideally before irreversible LV damage. Medical therapy (afterload reduction, diuretics) is a bridge.

Q4. Cardiac CT in a patient shows anomalous origin of left coronary artery from the pulmonary artery (ALCAPA). What are the risks and treatment?

Answer: The anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) leads to coronary steal, myocardial ischaemia, LV dysfunction, mitral regurgitation, and sudden death. The risks are high for heart failure in infancy and sudden cardiac death if left untreated. The treatment is surgical correction of the coronary anatomy (reimplantation of LCA into the aorta or Takeuchi procedure) to restore normal coronary perfusion.

Q5. On CMR you see late gadolinium enhancement in a mid-wall pattern in a young male with heart failure symptoms. What does this suggest and how does it affect prognosis?

Answer: Mid-wall late gadolinium enhancement on CMR in a non-ischaemic distribution suggests a non-ischaemic cardiomyopathy (e.g., dilated cardiomyopathy with fibrosis). This is associated with worse prognosis: higher risk of ventricular arrhythmias, sudden cardiac death, and worse response to therapy. It may influence decisions about implantable cardioverter-defibrillator (ICD) placement and closer follow-up.

Q6. In a nuclear SPECT stress scan you find reversible perfusion defects in the anterior wall and fixed defects in the inferior wall. What is interpretation and management?

Answer: Reversible perfusion defects indicate inducible ischaemia (viable myocardium at risk) in the anterior wall, while fixed defects represent scar (non-viable) in the inferior wall. Management: The anterior wall ischaemia indicates benefit from revascularisation (PCI or CABG) depending on coronary anatomy, functional capacity and comorbidities. The scarred inferior wall indicates previous infarction; guide medical therapy and consider ICD if LV dysfunction meets criteria.

Q7. On EP tracing you see a narrow QRS tachycardia that terminates with adenosine and on post-termination you see a short PR and delta wave. What is going on?

Answer: The narrow QRS tachycardia terminating with adenosine suggests a supraventricular tachycardia (SVT) mechanism. The post-termination finding of a short PR interval and delta wave suggests underlying accessory pathway (WPW). The mechanism of tachycardia is likely atrioventricular reciprocating tachycardia (AVRT) using the accessory pathway. Management: acute termination (adenosine intravenous) is correct; long-term management includes EP study and ablation of the accessory pathway to prevent future episodes and risk of rapid atrial fibrillation.

Q8. What are the indications for using CMR over echocardiography?

Answer: While echocardiography is first-line for structural assessment due to accessibility, CMR has advantages including superior image quality for complex anatomy, accurate quantification of volumes and ejection fraction, tissue characterisation (e.g., fibrosis via late gadolinium enhancement), assessment of myocarditis, cardiomyopathies, infiltrative diseases (e.g., amyloidosis, sarcoidosis) and viability. For patients in whom echo windows are poor or additional tissue information is needed, CMR is the modality of choice.

More Concepts commonly asked:

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🫀 FCPS Cardiology TOACS – Common Questions & Answers

🔹 ECG Interpretation Stations

Q1. A 12-lead ECG shows irregularly irregular rhythm, no distinct P waves, variable R-R intervals. What is the diagnosis and initial management?

A1. This is Atrial Fibrillation (AF). Initial management depends on stability:

Unstable (hypotension, chest pain, pulmonary edema): Immediate synchronized cardioversion.

Stable: Rate control (β-blocker, diltiazem, digoxin), anticoagulation assessment using CHA₂DS₂-VASc score, and plan for rhythm control if indicated.

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Q2. ST-segment elevation in II, III, aVF with reciprocal depression in I, aVL — diagnosis and management?

A2. Inferior wall STEMI due to right coronary artery occlusion.

Give aspirin + clopidogrel (or ticagrelor), heparin, high-dose statin, and immediate reperfusion (primary PCI preferred; if unavailable, thrombolysis).

Check for RV infarction (do right-sided leads). Avoid nitrates if RV involvement suspected.

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Q3. ECG shows wide-complex tachycardia at 160 bpm with AV dissociation and capture beats. Diagnosis and treatment?

A3. Sustained Monomorphic Ventricular Tachycardia (VT).

Stable: IV amiodarone or procainamide.

Unstable: Immediate synchronized cardioversion.

Long-term: Identify cause (ischemia, cardiomyopathy); consider ICD implantation.

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Q4. Prolonged QT interval followed by torsades-de-pointes episodes — what are the causes and management?

A4. Causes: Drugs (antiarrhythmics, macrolides, antipsychotics), electrolyte abnormalities (↓K⁺, ↓Mg²⁺, ↓Ca²⁺), congenital long QT.

Management: IV magnesium sulfate, correction of electrolytes, stop offending drugs, pacing if recurrent.

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Q5. ECG with deep Q waves in V1–V4 and persistent ST elevation months after MI — interpretation?

A5. Left Ventricular Aneurysm following anterior MI.

Confirm with echocardiography (akinetic/dyskinetic wall, possible thrombus). Treat with anticoagulation and consider surgery if heart failure or embolic risk.

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🔹 Chest X-Ray (CXR) Stations

Q6. CXR shows boot-shaped heart and decreased pulmonary vascular markings in a child — diagnosis?

A6. Tetralogy of Fallot. The boot shape is due to right ventricular hypertrophy; decreased pulmonary markings reflect pulmonary stenosis.

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Q7. CXR with “water-bottle-shaped” cardiac silhouette and clear lung fields — likely diagnosis?

A7. Pericardial Effusion. Confirm with echocardiography to assess effusion size and tamponade physiology.

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Q8. CXR showing rib notching and figure-of-3 sign — what is the diagnosis?

A8. Coarctation of Aorta. Rib notching due to collateral intercostal circulation; figure-of-3 from pre- and post-stenotic aortic dilatation.

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🔹 Echocardiography Stations

Q9. Echo shows concentric LV hypertrophy with small LV cavity and speckled myocardium. Diagnosis and next step?

A9. Suggestive of Restrictive Cardiomyopathy / Amyloidosis. Confirm with CMR (late gadolinium enhancement with diffuse subendocardial pattern). Treat underlying cause and manage heart failure with diuretics; avoid excessive preload reduction.

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Q10. Echo shows severe AS (aortic stenosis) — mean gradient 60 mmHg, valve area 0.6 cm², EF 45%. Management?

A10. Severe symptomatic aortic stenosis → definitive treatment is surgical AVR or TAVR (if high surgical risk). Medical therapy is supportive only.

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Q11. Echo shows large pericardial effusion with diastolic collapse of right atrium and ventricle. Diagnosis and management?

A11. Cardiac Tamponade. Immediate pericardiocentesis under echo guidance. Address underlying cause (infection, malignancy, uremia, etc.).

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Q12. Echo shows LV apical ballooning with hypercontractile base in a woman after emotional stress. Diagnosis?

A12. Takotsubo (Stress) Cardiomyopathy. Often mimics MI but coronary angiography shows normal arteries. Supportive care; usually reversible in weeks.

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🔹 Cardiac Catheterization / Angiography

Q13. Coronary angiogram shows left main stenosis >50%. What is the preferred management?

A13. CABG (Coronary Artery Bypass Grafting) is indicated for left main disease due to prognostic benefit.

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Q14. Cath report shows FFR = 0.74 in mid-LAD lesion. What does it mean?

A14. FFR < 0.80 indicates functionally significant stenosis → revascularization (PCI or CABG) is warranted.

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Q15. LV angiogram shows apical dyskinesia and basal hyperkinesia with normal coronaries. Diagnosis?

A15. Takotsubo Cardiomyopathy. Often triggered by emotional or physical stress. Manage supportively.

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🔹 Cardiac CT / CMR

Q16. CMR shows diffuse subendocardial late gadolinium enhancement and thickened myocardium. What is the diagnosis?

A16. Cardiac Amyloidosis. Characteristic diffuse enhancement pattern and difficulty nulling myocardium signal.

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Q17. Cardiac CT shows calcium score 1200 Agatston units. Interpretation?

A17. Very high coronary calcium burden → high risk for obstructive coronary disease; mandates aggressive risk factor control and further evaluation (stress test or CTA).

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Q18. CMR shows transmural LGE in LAD territory — what does it indicate?

A18. Non-viable scar tissue post-infarction; revascularization unlikely to improve function in that segment.

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🔹 EP (Electrophysiology) & Arrhythmias

Q19. EP tracing shows dual AV nodal pathways with echo beats. Diagnosis?

A19. AV Nodal Re-entrant Tachycardia (AVNRT). Slow-fast re-entry circuit; ablation of slow pathway is curative.

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Q20. EP study shows inducible sustained VT post-MI. What’s the implication?

A20. High risk of sudden cardiac death. ICD implantation is indicated for secondary prevention.

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Q21. Sinus pauses >3 seconds, alternating brady and tachy episodes on Holter — diagnosis and management?

A21. Tachy-Brady Syndrome (Sick Sinus Syndrome). Management: permanent pacemaker implantation if symptomatic.

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🔹 Nuclear Cardiology / Stress Imaging

Q22. Stress thallium scan shows reversible inferolateral defect with normal rest image. Interpretation?

A22. Reversible ischemia in inferolateral wall — viable myocardium at risk → consider coronary angiography and revascularization.

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Q23. PET scan shows preserved FDG uptake in hypoperfused segments. What does it mean?

A23. Viable but hibernating myocardium — likely to recover function after revascularization.

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Q24. Nuclear perfusion scan shows fixed anterior defect with LV dilatation and low EF. Interpretation?

A24. Old anterior MI with scar and remodeling. Management includes optimal medical therapy for HFrEF and ICD consideration if EF < 35%.

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🔹 Integrated Clinical Decision Questions

Q25. A patient presents with exertional dyspnoea, EF = 35%, QRS = 160 ms with LBBB morphology. Next best therapy?

A25. Cardiac Resynchronization Therapy (CRT) is indicated if symptomatic on GDMT, EF ≤ 35%, QRS ≥ 150 ms with LBBB pattern.

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Q26. A patient with dilated cardiomyopathy and EF = 25% asks about prognosis. What key factors affect it?

A26. Prognosis depends on NYHA class, EF, QRS duration, presence of fibrosis on CMR, and response to GDMT. ICD/CRT improve survival if indicated.

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Q27. After MI, patient develops hypotension, elevated JVP, and clear lungs. What should you suspect?

A27. Right Ventricular Infarction. Manage with volume loading, avoid nitrates, and treat underlying infarct (RCA occlusion).

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Q28. A young athlete has syncope during exercise; ECG shows deep inverted T waves in V1–V3. Diagnosis and test to confirm?

A28. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). Confirm with CMR showing RV dilation and fibrofatty infiltration. Advise exercise restriction and consider ICD.

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Q29. Post-valve surgery patient develops fever and new murmur. What is the investigation of choice?

A29. Transesophageal Echocardiography (TEE) — gold standard for detecting prosthetic valve endocarditis (vegetations, abscess).

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Q30. Patient on pacemaker presents with dizziness and cannon A-waves. Likely diagnosis?

A30. Pacemaker-Mediated Tachycardia or AV Dyssynchrony. Check pacemaker settings, perform device interrogation, and reprogram if needed.

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💡 Example Meta Description for Blog

> “Comprehensive guide for FCPS Cardiology TOACS preparation — includes ECG, Echocardiography, Cath Lab, CMR, CT, CXR, EP Tracings, and Nuclear Scans with commonly asked questions and answers. Perfect for FCPS Part 2 candidates in Pakistan from NICVD, AFIC, PIC, RIC, FIC, and other top cardiology training centers.”

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