A 25-year-old man attends the ED because of palpitations of 1 hour in duration. They occurred suddenly when he was watching TV. He says his heart feels as if it is racing extremely fast. The patient has never had similar symptoms before. He denies chest pain or shortness of breath. He has had no loss of consciousness. Vital signs: Temperature 98.6° F (37.0° C), pulse 205 beats/min, BP 110/80 mm Hg, RR 17 breaths/min. Additional history: No medical history. No use of drugs, tobacco, or alcohol.
What is the most likely cause of his palpitations?
Technically, SVT refers to any tachycardia that originates above the bundle of His (although it most commonly refers to AV nodal reentrant tachycardia [AVNRT]). AVNRT usually occurs spontaneously, although it may be triggered by stimulants, exercise, or alcohol. The most common presenting symptom is palpitations. Other symptoms such as chest pain and loss of consciousness represent unstable tachycardia and warrant a more aggressive approach. Because the patient is stable, vagal maneuvers such as the Valsalva maneuver can be attempted. If these fail, adenosine should be used to attempt to convert the heart to a sinus rhythm. Adenosine administration can be repeated three times. Adenosine is successful in inducing cardioversion in most cases. If it fails, however, an AV nodal blocking agent can be used such as a nondihydropyridine calcium channel blocker (diltiazem) or a beta-blocker (metoprolol). If at any point the patient becomes unstable (chest pain, hypotension, loss of consciousness), adenosine administration may be tried, but you should proceed quickly to synchronized cardioversion. A repeat ECG after the episode has resolved can screen for underlying dysrhythmias such as the preexcitation seen in Wolff-Parkinson-White syndrome. Patients with a single episode of well-tolerated AVNRT may not require any further treatment. Diltiazem and metoprolol are usually first-line agents for chronic suppressive therapy. In patients with poorly tolerated SVT, definitive management with catheter ablation should be considered. These decisions should be made in conjunction with a cardiologist. Patients with uncomplicated AVNRT without significant comorbidities may be discharged home with close cardiology follow-up. Poorly tolerated AVNRT or the presence of significant comorbidities probably warrants admission for monitoring.
A patient is diagnosed with long QT syndrome and has been commenced on beta-blockers with no symptoms and a QTc of 470 ms. No genetic testing has been performed. She has a 7-year-old daughter and asks about the risks for her child. What is it appropriate to tell her?
An increasing number of genes have been identified for the long QT syndrome but approximately 80% of patients have a mutation of one of three genes (LQT1–3). It is always best to perform genetic tests on the subject who has the clearest case of the condition. In this case, this is the patient herself. If a culprit gene can be found, the process of screening family members becomes much simpler.
A 61-year-old with a history of a myocardial infarction 2 years ago with a known ejection fraction of 25% presents to A&E with a 2 hour history of mild palpitations. He is otherwise fit and well. His ECG monitoring shows a regular broad complex tachycardia at a rate of 170 bpm which self-terminated before a 12-lead ECG was performed. His U&Es are normal. The patient’s blood pressure was 130/90 mmHg during the tachycardia and he was not unduly distressed. He is transferred to CCU where a 12-lead ECG shows LBBB with a QRS duration of 100 ms.
This man is very likely to have sustained ventricular tachycardia (VT) given his history of ischaemic heart disease, impaired ejection fraction, and broad complex tachycardia. The fact that he has tolerated it well is not an indication that it is an SVT, although this is possible. Therefore an ICD is indicated by NICE criteria as he has an EF <35%, sustained VT, ischaemic aetiology, and NYHA class III or less. It should be noted that this is a secondary prevention indication despite the fact the patient does not appear to have been compromised by his VT. NICE recommends a VT stimulation study for non-sustained VT (NSVT) and EF <35%, but the patient already meets criteria for an ICD and therefore this would be a redundant investigation. Flecainide is contraindicated in patients with established IHD or structural heart disease.
A patient with previous myocardial infarction, an ejection fraction of 25%, and a QRS duration of 140 ms, but no history of cardiac arrest, is seen in clinic and an ICD is recommended. She is concerned about driving. What is it appropriate to tell her?
The ICD would be a primary prevention device and therefore the patient needs to stop driving for 1 month (compared with 6 months for a secondary prevention device). However, if she has an appropriate shock it is then treated in the same way as a device implanted for secondary prevention and requires 6 months off driving.
Which one of the following features is least suggestive that a broad complex tachycardia is ventricular in origin (VT)?
P waves walking through the tachycardia and capture beats are evidence of independent P-wave activity and ‘prove’ that the rhythm is VT. If the QRS is broad in sinus rhythm, it indicates pre-existing conduction tissue disease which will not shorten if the tachycardia is an SVT. Therefore shortening of the QRS proves that the rhythm is VT, probably originating from the septum to give a relatively narrow QRS. Negative concordance shows that the rhythm is originating from the apex of the heart and is therefore VT. The rsR' pattern is seen in typical RBBB and is suggestive of aberrancy rather than VT, although this is not diagnostic.
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