Syncope Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Robert Harris is a 62-year-old accountant who presents with four episodes of syncope over the past 10 months. The episodes are unheralded — he has no prodrome — and they have occurred in various positions: twice while sitting at his desk, once while walking, and once while standing at a bus stop. He has a history of hypertension and a previous anterior myocardial infarction 4 years ago. He takes ramipril, bisoprolol, aspirin, and atorvastatin. On examination his blood pressure is 132/78, pulse 64 and regular. Cardiac auscultation is normal. His ECG shows sinus rhythm with right bundle branch block and left anterior fascicular block — bifascicular block — with Q waves in V1 to V4 consistent with his old anterior MI. His echocardiogram shows a left ventricular ejection fraction of 38 per cent with anterior wall motion abnormality. [1]

The critical issues are threefold. First, his syncope has no prodrome, which the 2018 ESC guidelines identify as a feature suggesting an arrhythmic mechanism. Second, he has structural heart disease with a reduced ejection fraction and bifascicular block on his ECG — both high-risk features. Third, the combination of previous MI, reduced LVEF, and bifascicular block puts him at significant risk of intermittent high-grade atrioventricular block or ventricular tachycardia as the cause of his syncope. My provisional diagnosis is arrhythmic syncope, and I would admit him for continuous ECG monitoring and expedited cardiac workup." [1]

Examiner: "What is the significance of the bifascicular block in this context?"

"Bifascicular block — right bundle branch block combined with left anterior fascicular block — indicates disease of two of the three fascicles of the His-Purkinje system. The third fascicle, the left posterior fascicle, is the sole remaining conduit for atrioventricular conduction. The 2018 ESC guidelines identify bifascicular block as a high-risk ECG finding in syncope because it carries a significant risk of progression to complete heart block, which can cause ventricular asystole and syncope or sudden death. [1]

In this patient, the risk is compounded by his structural heart disease — the previous anterior MI with reduced LVEF. The ischaemic substrate can damage the conduction system directly, and the scarred myocardium provides a substrate for ventricular tachycardia. The guidelines recommend that patients with syncope and bifascicular block undergo prolonged ECG monitoring, because the conduction disease may be intermittent and not apparent on a single 12-lead ECG." [1]

Examiner: "Walk me through your investigation plan."

"My investigation plan follows the ESC 2018 directed approach — the choice of test is guided by the initial evaluation, not applied as a blanket battery. [1]

First, the patient should be admitted for inpatient continuous telemetry monitoring. The priority is to detect intermittent high-grade AV block, sinus pauses, or ventricular tachycardia — the three arrhythmias that would explain his syncope and each require a different management strategy. If an arrhythmia is captured during admission, the diagnosis is made and I proceed to treatment. [1]

Second, if inpatient monitoring is negative, I would implant an implantable loop recorder. The episodes are infrequent — four in 10 months — and a Holter monitor of 24 to 48 hours has a very low yield. The ILR can monitor continuously for up to 3 years and has the best chance of capturing the rhythm at the time of syncope. The ISSUE-3 trial (PMID 22645283) demonstrated the importance of ILR documentation before committing to pacemaker therapy in suspected neurally mediated syncope — pacing was effective only when asystole was documented on the ILR. [1]

Third, I would perform an electrophysiology study. In a patient with structural heart disease, previous MI, and bifascicular block, an EP study can assess His-Purkinje conduction by measuring the HV interval — a prolonged HV interval (over 70 milliseconds) predicts progression to complete heart block. The EP study can also induce ventricular tachycardia, which would guide management toward an ICD. [1]

Fourth, I would repeat the echocardiogram to confirm the LVEF and assess for any interval change. An LVEF of 35 per cent or below would be an indication for a primary prevention ICD under current guidelines, independent of the syncope workup." [1]

Examiner: "The ILR records a 9-second asystolic pause with syncope, and the tilt test is negative. Carotid sinus massage is negative. What do you do?"

"This is a neurally mediated syncope with documented asystole — the exact population studied in the ISSUE-3 trial (PMID 22645283). ISSUE-3 randomised patients aged 40 or older with at least three episodes of severe neurally mediated syncope and documented asystole on ILR to dual-chamber pacing ON versus OFF. The 2-year syncope recurrence rate was 25 per cent with pacing ON versus 57 per cent with pacing OFF — a 57 per cent relative risk reduction. The subgroup analysis showed the benefit was actually greater when the tilt test was negative, which is exactly this patient. [1]

However, I must also consider his structural heart disease and reduced LVEF. The asystolic pause documented on the ILR could represent neurally mediated syncope (the Bezold-Jarisch reflex producing vagally mediated asystole), or it could represent intermittent complete heart block from his conduction system disease. The distinction matters because the management is different: a pacemaker is indicated for both, but if the LVEF is 35 per cent or below, he would also need an ICD for primary prevention of sudden cardiac death, regardless of the syncope mechanism. [1]

In this case, with an LVEF of 38 per cent, I would implant a dual-chamber pacemaker for the documented asystolic syncope. I would also have a detailed discussion about the risk of ventricular arrhythmia given his ischaemic substrate, and I would monitor his LVEF — if it declines to 35 per cent or below, I would upgrade to a CRT-D or ICD." [1]

Examiner: "What is the role of physical counter-pressure manoeuvres and pharmacotherapy in this patient?"

"Physical counter-pressure manoeuvres are first-line therapy for vasovagal syncope with a recognisable prodrome — the PC-Trial (PMID 17045903) showed a 39 per cent relative risk reduction. But this patient has no prodrome, which means he cannot anticipate the episodes and perform the manoeuvres. PCM is therefore not applicable in his case. [1]

Pharmacotherapy — fludrocortisone (POST2, PMID 27364043) and midodrine (POST4, PMID 34339231) — is intended for recurrent vasovagal syncope with a prodrome that has not responded to first-line measures. Again, this patient's presentation — no prodrome, documented asystole, structural heart disease — places him in the category where pacing is the evidence-based treatment, not pharmacotherapy." [1]

Short Case — Carotid Sinus Hypersensitivity

Examiner: "Describe your approach to carotid sinus massage and the interpretation of the response."

"Carotid sinus massage is indicated in patients over 40 with unexplained syncope suggestive of a reflex mechanism, after excluding a carotid bruit and recent TIA or stroke. The patient is positioned supine with continuous ECG and non-invasive blood pressure monitoring. I apply firm longitudinal pressure to the carotid bifurcation — at the level of the cricoid cartilage — for 5 to 10 seconds, first on the right then on the left after a 30-second rest. I also perform the massage in the upright position if the supine test is negative, as the sensitivity is higher upright. [1]

The test is positive if it produces a ventricular pause of 3 seconds or more (cardioinhibitory response), a systolic blood pressure drop of 50 mmHg or more (vasodepressor response), or both (mixed response) — and the response reproduces the patient's spontaneous symptoms. Carotid sinus syndrome is diagnosed when the response reproduces symptoms. [1]

The three response types determine management. The cardioinhibitory type responds to pacemaker therapy. The vasodepressor type does not — pacing cannot prevent reflex-mediated peripheral vasodilation, so management is avoidance of triggers and, if recurrent, midodrine. The mixed type is managed with pacing, as the cardioinhibitory component is the more amenable target. I should note that many patients with carotid sinus syndrome have amnesia for the loss of consciousness and present with unexplained falls rather than syncope — Parry et al. (PMID 19124530) demonstrated this important clinical point." [1]

Examiner: "What is the evidence for pacing in carotid sinus syndrome?"

"The evidence is stronger for patients presenting with syncope than for those presenting with unexplained falls. Open-label studies show a high reduction in recurrent syncope with pacing, but the few double-blinded studies have shown mixed results. The SAFE PACE 2 trial (PMID 20228148) randomised 141 patients with cardioinhibitory carotid sinus hypersensitivity and unexplained falls or syncope to pacing versus an implantable loop recorder. While the frequency of falls decreased after device implantation, there was no significant difference between the paced group and the control group. However, this trial included a high proportion of fallers rather than patients with clear syncope. [1]

The 2018 ESC guidelines (PMID 29860370) recommend cardiac pacing for patients with recurrent syncope and a cardioinhibitory or mixed carotid sinus response, acknowledging the evidence is stronger for syncope than for falls. The guidelines give pacing a class I recommendation for recurrent syncope attributable to carotid sinus syndrome with a cardioinhibitory response of 3 seconds or more." [1]

Examiner: "What is your prognosis for this patient?"

"It depends on the underlying mechanism and the success of treatment. For neurally mediated syncope with documented asystole treated with a pacemaker, the ISSUE-3 data show a 2-year syncope recurrence rate of 25 per cent — a significant improvement but not a complete cure, because the vasodepressor component may persist. For carotid sinus syndrome treated with pacing, the prognosis is generally good with low recurrence rates. [1]

The broader prognostic concern in this patient is his structural heart disease — the previous MI with reduced LVEF. Even if the syncope mechanism is neurally mediated and treated with a pacemaker, his ischaemic substrate carries an ongoing risk of ventricular arrhythmia and sudden cardiac death. I would monitor his LVEF, optimise his heart failure medical therapy, and ensure he meets the threshold for primary prevention ICD if his LVEF declines to 35 per cent or below. The single most important prognostic factor is the state of his left ventricle, not the syncope mechanism itself." [1]