Keeled over carrying the shopping

A 79-year-old man is brought in by ambulance after losing consciousness while walking uphill with his shopping bags. He was back to himself within a minute, with no tongue biting or incontinence. Over the past few months he has noticed worsening breathlessness on hills and one episode of chest heaviness on exertion that settled with rest. He takes amlodipine for hypertension.

Stage 1 of 3

His arrival ECG is recorded.

Tracing 1 of 2 for the quiz “Keeled over carrying the shopping”. — 12-lead, 25 mm/s, 10 mm/mV Open this tracing in the studio

Observations

BP: 112/86 mmHg
RR: 18
SpO2: 96% on air
Temp: 36.7 °C
Heart rate: 66 bpm

Bloods

hs-troponin T: 38 ng/L (upper limit of normal 14)

What is the most likely explanation for the ECG findings?

ALeft ventricular hypertrophy with strain Correct answer Your answer
BLateral non-ST elevation myocardial infarction Your answer
CDiffuse subendocardial ischaemia Your answer
DDigoxin effect Your answer

There is high QRS voltage across the precordial leads, with deep S waves in V2 and V3 and tall R waves in V4 and V5. The downsloping ST depression and asymmetric T inversion in I, II and V4 to V6, with ST elevation in aVR and V1, are the repolarisation abnormality of left ventricular hypertrophy rather than an acute ischaemic change. The pattern of widespread depression with aVR elevation can mimic diffuse subendocardial ischaemia from left main or three-vessel disease, but here the depression follows the leads with dominant R waves and the T waves have the asymmetric downslope of strain. Digoxin produces a scooping morphology quite unlike this pattern.

Given the history of exertional syncope and this ECG, what is the single most useful next investigation?

ATransthoracic echocardiography Correct answer Your answer
BCT head Your answer
CTilt table testing Your answer
DUrgent coronary angiography Your answer

Exertional syncope in an elderly patient with ECG evidence of significant left ventricular hypertrophy points to a structural cause, most likely aortic stenosis. Echocardiography will quantify the valve disease and ventricular function in minutes. CT head adds nothing when the history is clearly cardiac syncope with prompt recovery, and tilt table testing is for vasovagal syncope without a structural explanation. Coronary angiography may follow, but the mildly raised troponin with a strain pattern is not an indication for emergency catheterisation.

Stage 2 of 3

On examination you find a harsh ejection systolic murmur radiating to the carotids with a slow-rising pulse. The bedside echocardiogram shows severe calcific aortic stenosis with a peak velocity of 4.6 m/s, mean gradient 48 mmHg, valve area 0.7 cm squared, concentric left ventricular hypertrophy with a septal thickness of 15 mm and a preserved ejection fraction of 60%. The admitting team has written up for a presumed non-ST elevation myocardial infarction and is about to start a glyceryl trinitrate infusion for the exertional chest heaviness.

What is the most important hazard in his immediate management?

AGTN causing hypotension in fixed obstruction Correct answer Your answer
BUnfractionated heparin causing bleeding Your answer
CAspirin worsening a cerebral event Your answer
DIntravenous fluid overload Your answer

In severe aortic stenosis the cardiac output is fixed by the valve, and systemic vascular resistance is what maintains the coronary and cerebral perfusion pressure. Glyceryl trinitrate reduces both preload and afterload, which in this setting can cause profound and refractory hypotension. The pulse pressure is already narrow at 112/86 mmHg. Heparin and aspirin carry their own risks but are not the immediate life threat here, and a cautious fluid challenge is more likely to help than to harm in a preload-dependent ventricle.

Stage 3 of 3

Two hours later he becomes acutely grey and light-headed with palpitations. His blood pressure is 78/50 mmHg. A repeat ECG is recorded.

Tracing 2 of 2 for the quiz “Keeled over carrying the shopping”. — 12-lead, 25 mm/s, 10 mm/mV Open this tracing in the studio

Observations

BP: 78/50 mmHg
Heart rate: 146 bpm

What is the best immediate management?

ASynchronised DC cardioversion Correct answer Your answer
BIntravenous amiodarone over 20 to 60 minutes Your answer
CIntravenous metoprolol Your answer
DIntravenous diltiazem Your answer

The ECG shows atrial fibrillation with a rapid ventricular rate. In a patient with severe aortic stenosis and concentric left ventricular hypertrophy, the loss of organised atrial contraction is catastrophic: the stiff ventricle depends on atrial contraction for a much larger share of its filling than a normal one, and the tachycardia shortens diastolic filling time further. Hypotension with signs of shock is an adverse feature, and it mandates immediate synchronised DC cardioversion. Diltiazem is a vasodilator and negative inotrope and is particularly dangerous here. Amiodarone and beta-blockers may be considered once haemodynamic stability is restored, but waiting 20 to 60 minutes for a pharmacological effect in this setting risks cardiac arrest.

Diagnosis

Severe calcific aortic stenosis with left ventricular hypertrophy and strain, decompensated by atrial fibrillation

The first ECG shows left ventricular hypertrophy with a strain pattern: deep precordial S waves, tall lateral R waves meeting voltage criteria, and downsloping ST depression with asymmetric T inversion across the lateral and inferior leads, with reciprocal ST elevation in aVR and V1. The combination of widespread ST depression and aVR elevation is easily mistaken for diffuse subendocardial ischaemia, but here the depression follows the leads with dominant R waves and the T wave morphology is the asymmetric downslope of strain rather than the symmetric inversion of ischaemia. Strain and ischaemia can coexist and cannot always be separated on a single tracing, but the second ECG recorded during atrial fibrillation at 146 beats per minute shows an identical ST pattern, which argues against a rate-dependent ischaemic change. The mildly raised troponin is more likely the strain of a pressure-loaded ventricle than an acute coronary syndrome. Exertional syncope in an elderly patient with this ECG pattern should prompt echocardiography before any other investigation.

The bedside echo confirms severe calcific aortic stenosis. The immediate hazard is vasodilator therapy: glyceryl trinitrate or calcium channel blockers reduce preload and afterload against a fixed obstruction, risking cardiovascular collapse. When atrial fibrillation then removes the atrial contribution to filling a stiff, hypertrophied ventricle, the result is acute haemodynamic compromise. With adverse features present, synchronised DC cardioversion is the correct first step.

References

Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2022;43(7):561-632.
Hancock EW, Deal BJ, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy. Circulation. 2009;119(10):e251-e261.
Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support. Resuscitation. 2021;161:115-151.

Keeled over carrying the shopping

The case

On arrival

Observations

Bloods

Observations

Diagnosis

References

Discussion