Syncope — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Harris, 62 years old, accountant. [1]

Presenting complaint: Four episodes of loss of consciousness over the past 10 months. [1]

History of presenting complaint:

• First episode: 10 months ago, while sitting at his desk reviewing accounts. No warning. Colleagues found him slumped in his chair, pale. He recovered within 30 seconds and was immediately orientated. He did not bite his tongue or lose bladder control.
• Second episode: 7 months ago, while walking to the bus stop after work. He felt nothing before it, simply collapsed. A passer-by called an ambulance. He recovered by the time paramedics arrived (approximately 2 minutes). Blood glucose was normal.
• Third episode: 3 months ago, while standing at the bus stop. Again no prodrome. He fell, grazing his forehead. Recovered within 1 minute.
• Fourth episode: 2 weeks ago, while sitting at his desk again. No warning. Colleague witnessed pallor and a brief irregular jerking of his arms lasting approximately 5 seconds. Recovered within 30 seconds.
• No chest pain, palpitations, dyspnoea, or neurological symptoms preceding or following any episode. No incontinence, no tongue biting, no postictal confusion. [1]

Past medical history:

• Anterior myocardial infarction 4 years ago, treated with primary PCI (stent to LAD)
• Hypertension for 15 years
• No diabetes, no known structural valve disease [1]

Medications: Ramipril 10 mg daily, bisoprolol 5 mg daily, aspirin 100 mg daily, atorvastatin 80 mg daily. [1]

Family history: Father died at 74 from stroke. No family history of sudden cardiac death. No known inherited cardiac conditions. [1]

Social history: Married, works as an accountant. Drives a private vehicle. Does not smoke. Drinks 2 standard drinks on weekends. [1]

Examination:

• Blood pressure 132/78 (both arms equal), pulse 64 and regular
• JVP not elevated
• Heart sounds normal, no murmurs, no gallop
• Chest clear
• No focal neurological signs
• No carotid bruit [1]

Investigations:

• ECG: sinus rhythm, right bundle branch block with left anterior fascicular block (bifascicular block), Q waves V1 to V4, QTc 420 ms
• Echocardiogram: LVEF 38 per cent, anterior wall hypokinesia, mild LV dilatation, no significant valvular disease, no RV dysfunction
• Bloods: Hb 142, Na 140, K 4.2, Cr 88, eGFR 88, troponin negative, HbA1c 5.6 per cent [1]

Candidate's structured presentation (model answer)

"Mr Harris is a 62-year-old accountant with four episodes of unheralded syncope over 10 months, in the context of a previous anterior myocardial infarction with a reduced ejection fraction of 38 per cent and bifascicular block on his ECG. The episodes have no prodrome, occur in various positions including sitting and standing, and are associated with pallor and brief myoclonic jerking but no postictal confusion, tongue biting, or incontinence. [1]

The key issues are: first, whether this is syncope or seizure — the rapid recovery without postictal confusion strongly favours syncope. Second, the ESC 2018 classification — the absence of a prodrome, the occurrence while sitting, and the structural heart disease with bifascicular block all point toward a cardiac, likely arrhythmic, mechanism. Third, the risk stratification — this patient has multiple high-risk features including structural heart disease with reduced LVEF, abnormal ECG with bifascicular block, and recurrent episodes causing injury. He requires admission for continuous ECG monitoring and expedited cardiac workup." [1]

Examiner questions and model answers

"What is your differential diagnosis and what is the most likely mechanism?" [1]

"The differential is between arrhythmic syncope (intermittent high-grade AV block from the bifascicular block, or ventricular tachycardia from the ischaemic substrate) and neurally mediated syncope with asystole. The absence of a prodrome favours an arrhythmic mechanism over reflex syncope. The occurrence while sitting excludes orthostatic hypotension. The bifascicular block on ECG is the strongest clue — it indicates disease of two of the three fascicles of the His-Purkinje system, with the third (left posterior fascicle) being the sole remaining conduit for AV conduction. Intermittent complete heart block is a real risk. [1]

However, I cannot exclude a neurally mediated mechanism — the ISSUE-3 trial demonstrated that patients with presumed neurally mediated syncope and documented asystole can have structural heart disease, and the tilt test is often negative in this population. The ILR is the tool that will distinguish between these mechanisms by documenting the rhythm at the time of syncope." [1]

"What investigations would you arrange?" [1]

"Admission for inpatient continuous telemetry is the first priority. If no arrhythmia is captured during admission, an implantable loop recorder is indicated — the episodes are infrequent (four in 10 months), and a Holter monitor of 24 to 48 hours has a very low diagnostic yield. The ILR can monitor for up to 3 years. [1]

An electrophysiology study should be considered to evaluate His-Purkinje conduction (HV interval) and assess for inducible ventricular tachycardia, given the ischaemic substrate. A prolonged HV interval (over 70 milliseconds) would predict progression to complete heart block and support prophylactic pacing. [1]

I would also consider repeating the echocardiogram in 3 months — if the LVEF has declined to 35 per cent or below, he would meet the criteria for a primary prevention ICD regardless of the syncope mechanism." [1]

"The ILR documents a 9-second asystolic pause with syncope. The tilt test is negative. What is your diagnosis and management?" [1]

"The diagnosis is neurally mediated syncope with documented asystole, confirmed by the ILR. The negative tilt test is actually consistent with this — the ISSUE-3 subgroup analysis showed the benefit of pacing was greater when the tilt test was negative. The 9-second asystolic pause exceeds the ISSUE-3 threshold of 3 seconds with syncope. [1]

My management is dual-chamber pacemaker implantation. ISSUE-3 (PMID 22645283) randomised patients aged 40 or older with at least three episodes of neurally mediated syncope and documented asystole on ILR to pacing ON versus OFF. The 2-year syncope recurrence was 25 per cent versus 57 per cent — a 57 per cent relative risk reduction. [1]

I must also address his LVEF of 38 per cent. While this does not meet the threshold for a primary prevention ICD (35 per cent or below), I would optimise his heart failure therapy — ensure he is on an ACE inhibitor (he is on ramipril), a beta-blocker (he is on bisoprolol), and consider adding an MRA (e.g., spironolactone or eplerenone) and an SGLT2 inhibitor. I would monitor his LVEF — if it declines, ICD evaluation is warranted." [1]

"What driving advice would you give?" [1]

"Mr Harris drives a private vehicle. Per the Austroads guidelines, after unexplained syncope, he should not drive for a minimum of 4 weeks from the last episode. Once a pacemaker is implanted and confirmed functional, and assuming no further syncope, he may resume private driving after approximately 1 week post-implantation. If he were a commercial driver, the restriction would be much more prolonged — he would need a definitive treatable cause and successful treatment before returning to commercial driving." [1]

Short Case — Carotid Sinus Hypersensitivity

Patient brief

Patient: Mr William Chen, 78 years old, retired teacher. [1]

Presenting complaint: Three episodes of syncope over 6 months, each while turning his head to reverse his car or while shaving with a tight collar. [1]

History: No prodrome. Rapid recovery. No palpitations, chest pain, or exertional symptoms. [1]

Past medical history: Hypertension, BPH. No diabetes, no known heart disease. [1]

Medications: Irbesartan 150 mg daily, tamsulosin 0.4 mg nightly. [1]

Examination: BP 138/82, pulse 72 and regular. No murmurs. No carotid bruit. No focal neurological signs. [1]

ECG: Normal sinus rhythm, normal intervals, no ischaemic changes. [1]

Echocardiogram: Normal LV function, no significant valvular disease. [1]

Examiner questions and model answers

"What is your provisional diagnosis and what test would confirm it?" [1]

"The provisional diagnosis is carotid sinus syndrome. The episodes are triggered by head turning and a tight collar — classic mechanical stimulation of the carotid sinus. The patient is an older man (the typical demographic, with a male-to-female ratio of approximately 4 to 1), and the episodes occur without a prodrome, which is characteristic. 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]

The test is carotid sinus massage, performed with the patient supine and monitored with continuous ECG and non-invasive blood pressure. I would first auscultate for a carotid bruit — if present, or if there is a history of recent TIA or stroke, the test is contraindicated. I would apply firm 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 would also perform the massage in the upright position if the supine test is negative, as sensitivity is higher upright. [1]

The test is positive if it produces a ventricular pause of 3 seconds or more (cardioinhibitory), a systolic blood pressure drop of 50 mmHg or more (vasodepressor), or both (mixed), AND reproduces the patient's symptoms." [1]

"Carotid sinus massage produces a 6-second ventricular pause with reproduction of his symptoms. The blood pressure drops 20 mmHg systolic. What is your interpretation and management?" [1]

"The response is cardioinhibitory — the 6-second ventricular pause exceeds the 3-second threshold, and the blood pressure drop of 20 mmHg is below the 50 mmHg threshold for a vasodepressor response. The symptoms are reproduced, confirming carotid sinus syndrome with a cardioinhibitory response. [1]

The management is permanent dual-chamber pacemaker implantation. The 2018 ESC guidelines (PMID 29860370) give a class I recommendation for cardiac pacing in patients with recurrent syncope attributable to carotid sinus syndrome with a cardioinhibitory response of 3 seconds or more. Pacing is effective for the cardioinhibitory type because it prevents the asystole that causes the syncope. [1]

I would also advise the patient to avoid tight collars and to be cautious with head turning, particularly when driving. He should not drive until the pacemaker is implanted and confirmed functional. I would review his medications — tamsulosin is a selective alpha-1A blocker with less effect on blood pressure than non-selective alpha-blockers, but I would still check his orthostatic blood pressure to ensure there is no additional orthostatic component." [1]

"What if the response had been purely vasodepressor — a 60 mmHg systolic drop without significant bradycardia?" [1]

"Then the management would be different. Pacing does NOT help the vasodepressor type of carotid sinus syndrome, because the mechanism is reflex-mediated peripheral vasodilation, not asystole. A pacemaker cannot prevent the fall in blood pressure from vasodilation. [1]

Management of the vasodepressor type is avoidance of triggers (tight collars, head turning), and if recurrent, pharmacological therapy to support blood pressure — midodrine, an alpha-1 agonist that increases venous return and blood pressure. The POST4 trial (PMID 34339231) demonstrated that midodrine significantly reduced syncope recurrence in vasovagal syncope, and the mechanism is analogous in the vasodepressor type of carotid sinus syndrome. I would also check for and address any orthostatic component with medication review and non-pharmacological measures." [1]

"What is the prognosis for this patient?" [1]

"With a cardioinhibitory carotid sinus syndrome treated with a pacemaker, the prognosis is generally very good. Open-label studies show a high reduction in recurrent syncope with pacing. The main caveat is from the SAFE PACE 2 trial (PMID 20228148), which found no significant difference between pacing and an implantable loop recorder in patients presenting with unexplained falls — but this patient has clear syncope, not falls, and the evidence is stronger for syncope. His overall prognosis is also favourable because he has no structural heart disease and a normal ECG, which distinguishes him from the previous long-case patient with ischaemic cardiomyopathy." [1]