Undifferentiated Palpitations — Viva

Short Case Viva Defence

Examiner instruction

"This patient has been referred with palpitations. Take a focused history, perform the relevant examination, present your findings, and discuss your approach." [1]

Candidate's model history and examination

"Before I begin, I would like to introduce myself, explain the assessment, and obtain consent. I would ensure good natural light and privacy. [1]

First, I will take a focused history of the palpitations. I want to know the character of the sensation — is it fast and regular (suggesting SVT or sinus tachycardia), fast and irregular (suggesting AF or flutter with variable block), a missed beat or an extra beat (suggesting ectopics), or a pounding or forceful sensation in a regular rhythm (suggesting an increased stroke volume from anaemia, thyrotoxicosis, pregnancy, fever, or aortic regurgitation)? I want to know the onset — sudden (suggesting a re-entrant tachycardia) or gradual (suggesting sinus tachycardia). I want to know the duration and the termination — the sudden offset suggests the SVT, and the termination followed by a brisk polyuria is the SVT discriminator. I want to know the triggers — the exercise (the red flag for the VT and the channelopathies), the caffeine, the alcohol, the stress. I want to know the associated symptoms — the syncope (the red flag), the chest pain, the dyspnoea, the polyuria. I want to know the drug history — the salbutamol, the decongestants, the thyroxine, the QT-prolonging drugs. I want to know the family history — the sudden cardiac death under 40 (the channelopathies, the cardiomyopathies). And I want to know the past cardiac history — the prior infarction, the cardiomyopathy, the valve disease. [1]

On general inspection, the patient is comfortable at rest, with no pallor, no flushing, no distress. [1]

The vital signs: the pulse is irregularly irregular at 85 beats per minute, with an apex rate of 95 — the apex-radial deficit is consistent with atrial fibrillation. The blood pressure is 145 over 90. The respiratory rate is 16. The oxygen saturation is 98 per cent on room air. [1]

The jugular venous pressure is not elevated. [1]

The apex beat is not displaced and is of normal character. There is no right ventricular heave. [1]

On auscultation, the first and second heart sounds are normal, with no added sounds and no murmurs. [1]

The thyroid examination reveals a smooth, firm, non-tender goitre of approximately 40 grams, with a soft bruit over the right lobe. There is no exophthalmos, no lid retraction, and no lid lag. [1]

The chest is clear. There is no peripheral oedema. [1]

In summary, this patient has atrial fibrillation with an underlying smooth goitre and a thyroid bruit — the findings are consistent with the thyrotoxic AF from the suspected Graves disease. I would like to check the full blood count, the thyroid function with the TSH and the free T4 and the thyroid antibodies, the urea and electrolytes, and I would organise an echocardiogram. I would assess the stroke risk with the CHA2DS2-VASc score and the bleeding risk with the HAS-BLED score, and I would initiate the appropriate management — the rate control with a beta-blocker and the anticoagulation, with the treatment of the underlying thyrotoxicosis." [1]

Examiner probing questions and model answers

Q1: "How do you classify the palpitations from the history, and why does this matter?" [1]

"The classification uses four descriptors derived from the symptom character: the regular fast rhythm (the sinus tachycardia, the SVT, the VT), the irregular rhythm (the AF, the flutter with the variable block, the frequent ectopics), the missed beat or the extra beat sensation (the ectopics), and the pounding or the forceful sensation in the regular rhythm (the anaemia, the thyrotoxicosis, the pregnancy, the fever, the aortic regurgitation, the MVP, the anxiety, the sympathomimetics). This matters because each descriptor points to a small set of diagnoses, each with the discriminating features that the history and the ECG confirm, and the classification narrows the differential before any test is ordered. The history is the most powerful investigation in the palpitations encounter — the ECG confirms what the history suspects, and the ambulatory monitoring captures what the ECG between episodes misses." [1]

Q2: "What are the high-risk features that mandate the urgent cardiology referral?" [1]

"The five high-risk features are: first, the syncope or the near-syncope during the palpitations — the cerebral hypoperfusion from a haemodynamically compromising tachycardia. Second, the exertional symptoms — the VT, the channelopathies (the LQT1 triggered by the exercise, the CPVT triggered by the exercise and the emotion), and the structural disease (the HCM, the aortic stenosis). Third, the family history of the sudden cardiac death under the age of 40 — the inherited arrhythmia syndromes (the long QT, the Brugada, the CPVT, the ARVC, the HCM). Fourth, the structural heart disease — the prior infarction, the cardiomyopathy, the heart failure. Fifth, the abnormal ECG — the long QT, the Brugada pattern, the epsilon wave, the right precordial T-wave inversions, the pathological Q waves, the LVH with the strain. Any of these mandates the urgent cardiology referral, the echocardiogram, the ambulatory monitoring, and the consideration of the EP study and the ICD [5][8]."

Q3: "A 24-year-old man presents with a short PR interval and a delta wave on the ECG. What is the diagnosis, and what is the management?" [1]

"The diagnosis is the Wolff-Parkinson-White syndrome — the accessory pathway (the bundle of Kent) connecting the atrium to the ventricle and bypassing the AV node, producing the pre-excitation (the delta wave) and the short PR interval. The significance is the risk of the sudden cardiac death — if the patient develops the AF, the rapid conduction down the accessory pathway can degenerate into the VF. The risk is determined by the antegrade effective refractory period of the accessory pathway, measured at the EP study — the short ERP (less than 250 milliseconds) identifies the high-risk patient. The management is the referral to the cardiac electrophysiology service for the risk stratification and the catheter ablation of the pathway, which is curative. The critical safety point: the AV nodal blockers (the verapamil, the adenosine, the beta-blocker, the digoxin) are contraindicated in the patient with the WPW and the AF, because they block the AV node preferentially and accelerate the conduction down the accessory pathway, increasing the VF risk [1][7][8]."

Q4: "What is the modified Valsalva manoeuvre, and what was the finding of the REVERT trial?" [1]

"The modified Valsalva manoeuvre is the postural modification of the standard Valsalva for the emergency termination of the SVT. The technique: the patient blows into a 10 mL syringe to move the plunger (generating approximately 40 mmHg of pressure) for 15 seconds in the semi-recumbent position (at 45 degrees), then the operator immediately repositions the patient supine with the legs passively raised at 45 degrees for 15 seconds. The passive leg raise augments the venous return and the vagal tone at the moment of the release, increasing the AV nodal block. The REVERT trial (the Randomised Evaluation of modified Valsalva Effectiveness in Re-entrant Tachycardias, Appelboam et al., Lancet 2015) randomised 433 patients to the modified versus the standard Valsalva and found the return to the sinus rhythm at 60 seconds in 43 per cent of the modified group versus 17 per cent of the standard group — an absolute difference of 26 per cent and a number needed to treat of approximately 4. The modified Valsalva is now the recommended first manoeuvre for the SVT termination [4]."

Q5: "Why must you not give adenosine or verapamil to a broad-complex tachycardia?" [1]

"Because if the broad-complex tachycardia is the ventricular tachycardia, the AV nodal blocking agent does not terminate the rhythm (the circuit is below the AV node) and may precipitate the haemodynamic collapse — the verapamil is a negative inotrope and a vasodilator, and the patient with the VT is often already haemodynamically compromised. The adenosine-induced vasodilatation in the poor cardiac reserve can precipitate the collapse, and the adenosine may provoke the VF in the VT patient. The correct approach is to treat the broad-complex tachycardia as the VT until proven otherwise — the synchronised DC cardioversion if unstable, the intravenous amiodarone or the procainamide if stable. The adenosine has a small diagnostic role — if it terminates the rhythm, the diagnosis is the SVT — but it must not be given if there is any reasonable possibility of the VT. The principle: treat every broad-complex tachycardia as the VT until proven otherwise [6]."

Q6: "How do you match the ambulatory ECG monitoring to the frequency of the symptoms?" [1]

"The ambulatory monitoring is matched to the frequency of the symptoms because the diagnostic yield is directly proportional to the match. The 24-hour Holter for the daily symptoms — the recording window captures the episode. The patient-activated event monitor (the cardio-memo, the external loop recorder) or the 14-day patch recorder (the Zio XT) for the weekly symptoms — the extended window and the patient activation increase the yield. The implantable loop recorder (the ILR, the Reveal LINQ, the Confirm RX) for the monthly or the rarer symptoms, or the unexplained syncope with the suspected arrhythmic cause — the device monitors continuously for up to three years and transmits the recorded events. A 24-hour Holter for the patient whose palpitations come every two months is wasted effort — the diagnostic yield is near zero. The principle: match the monitoring to the frequency [2][1] />."

Exam traps

The "normal ECG excludes the arrhythmia" trap: a normal ECG between episodes does not exclude an arrhythmia — it is normal in up to half of the patients with a documented arrhythmia. The ECG may, however, reveal the substrate (the delta wave, the long QT, the Brugada pattern, the LVH, the old Q waves). The candidate who is reassured by a normal ECG without the ambulatory monitoring has missed the diagnosis. [1]

The "broad-complex tachycardia is SVT with aberrancy" trap: the broad-complex tachycardia is VT until proven otherwise, especially in the patient with the structural heart disease. The AV nodal blockers that terminate the SVT may precipitate the collapse in the VT. Treat as VT until proven otherwise. [1]

The "Holter for the infrequent palpitations" trap: the 24-hour Holter for the monthly palpitations is wasted effort. Match the monitoring to the frequency — the event monitor or the patch recorder for the weekly, the ILR for the monthly or the rarer. [1]

The "sinus tachycardia is benign" trap: the sinus tachycardia is a physiological response to a stimulus, but the stimulus may be serious (the sepsis, the pulmonary embolism, the thyrotoxicosis, the phaeochromocytoma). Exclude the systemic causes before attributing the sinus tachycardia to the anxiety. [1]