Tachyarrhythmias

Definition and classification. A tachyarrhythmia is a rhythm with a ventricular rate above 100 beats per minute. Classify first by QRS width — this is the practical bedside division: Narrow complex (QRS < 120 ms) — supraventricular Broad complex (QRS ≥ 120 ms) Sinus tachycardia; atrial fibrillation; atrial flutter; atrial Ventricular tachycardia (monomorphic or polymorphic); tachycardia; multifocal atrial tachycardia (classically in COPD); torsades de pointes; ventricular fibrillation; SVT with aberrant AV nodal re-entrant tachycardia (AVNRT); AV re-entrant conduction or pre-existing bundle branch block; pre-excited AF; tachycardia (AVRT) paced rhythm Any broad-complex tachycardia in an older patient with structural heart disease must be treated as ventricular tachycardia until proved otherwise.

Epidemiology and substrate in old age. Abnormal heart rhythm increases with age even in those with normal hearts — the prevalence of atrial and ventricular ectopy reaches up to 100% in older people, and ventricular arrhythmias can be found in 70–80% of people over 60. Age-related fibrosis of the conduction system and atrial myocardium, chamber dilatation, ischaemic scar and hypertrophy provide the substrate. For a ventricular tachyarrhythmia to develop, both a substrate — structural (infarcted or hypertrophic myocardium creating myocytes of differing refractory periods and a re-entrant circuit) or electrical (early or delayed after-depolarisations) — and a trigger are required; the trigger is typically transient, such as electrolyte imbalance, acute ischaemia or an antiarrhythmic drug (as in torsades de pointes). Channelopathies such as congenital long QT and Brugada syndrome are uncommon in older age groups.

Clinical features. Palpitations, breathlessness, chest pain, dizziness, presyncope, syncope or, in sustained VT, cardiac arrest. In older patients presentation is frequently atypical — falls, confusion, fatigue, decompensated heart failure or an incidental finding. Assess haemodynamic stability immediately, looking for the adverse features: shock, syncope, myocardial ischaemia and heart failure. Examine for cannon 'a' waves and variable intensity of the first heart sound, which indicate AV dissociation and therefore VT.

Diagnosis. Obtain a 12-lead ECG during the tachycardia wherever possible, plus a rhythm strip; a previous ECG in sinus rhythm is invaluable for comparison. ECG features favouring VT over SVT with aberrancy: AV dissociation, capture and fusion beats, QRS > 140 ms, extreme (northwest) axis, concordance across the precordial leads, and a history of previous myocardial infarction — the last being the single most useful clinical discriminator. For intermittent arrhythmia use Holter monitoring, an event recorder, an implantable loop recorder or wearable ECG. Always check potassium, magnesium, calcium, renal and thyroid function, troponin and digoxin level, review the drug chart for QT-prolonging agents, and obtain an echocardiogram. Interpretation of asymptomatic rhythm disturbance is difficult in the old, since minor asymptomatic dysrhythmias are common and may be entirely incidental — symptom–rhythm correlation is essential.

Acute management. The decision is driven by haemodynamic stability. UNSTABLE (shock, syncope, ischaemia, heart failure) → immediate synchronised DC cardioversion under sedation (unsynchronised defibrillation for VF or pulseless VT) STABLE narrow-complex → vagal manoeuvres → adenosine 6 mg then 12 mg rapid IV bolus (contraindicated in asthma); if AF or flutter, rate control with a beta-blocker or diltiazem STABLE broad-complex → treat as VT: amiodarone 300 mg IV over 20–60 min then 900 mg/24 h; correct electrolytes Torsades de pointes → IV magnesium sulphate 2 g, stop the offending drug, correct K+, overdrive pacing or isoprenaline Never give verapamil or diltiazem to a broad-complex tachycardia — if it is VT, the result may be cardiovascular collapse. Always correct potassium and magnesium and treat the underlying trigger — ischaemia, sepsis, hypoxia, thyrotoxicosis, anaemia or drug toxicity.

Long-term management and prognosis. Treat the underlying disease — revascularisation for ischaemia, optimal heart failure therapy, correction of electrolytes, withdrawal of proarrhythmic and QT-prolonging drugs. Beta-blockers are the antiarrhythmic backbone; amiodarone is the most usable agent in structural heart disease but carries thyroid, hepatic, pulmonary, corneal and neurological toxicity in long-term use; flecainide and propafenone are restricted to structurally normal hearts. Catheter ablation is curative for AVNRT, AVRT and atrial flutter and is effective for scar-related VT. ICD for secondary prevention after sustained VT or aborted sudden cardiac death, and for primary prevention with a reduced ejection fraction — pooled trial data show the survival benefit of the primary-prevention ICD persists in older patients, but the decision must weigh life expectancy, frailty and patient wishes, and ICD deactivation must be discussed as part of end-of-life planning. On prognosis: ventricular ectopy and non-sustained VT in the absence of heart disease are not associated with increased coronary disease or mortality and do not require antiarrhythmic drugs; there is no association between the extent or complexity of ventricular ectopy and coronary disease in the absence of left ventricular dysfunction, and prognosis is good. By contrast, polymorphic VT is a risk marker even without heart disease, and after myocardial infarction frequent ectopy (> 10/hour), runs of ectopy or non-sustained VT with a reduced ejection fraction are independently associated with new coronary events and mortality. Ventricular arrhythmias in the first 24–48 hours after acute myocardial infarction do not indicate continuing risk.

Wearable and consumer devices have become a routine part of arrhythmia diagnosis. Following large screening studies (Apple Heart, Fitbit Heart, mSToPS, LOOP), smartwatch and single-lead handheld ECG devices are now accepted for symptom–rhythm correlation and for confirming AF, and the 2024 ESC AF guideline explicitly addresses device-detected atrial high-rate episodes. The key examinable nuance comes from NOAH-AFNET 6 (NEJM 2023) and ARTESiA (NEJM 2023), which studied subclinical device-detected atrial fibrillation: anticoagulation produced only a small reduction in stroke that was largely offset by an increase in major bleeding. The conclusion is that device-detected subclinical AF is NOT equivalent to clinical AF, and should not automatically trigger anticoagulation — a decision that requires individual assessment of episode duration, stroke risk and bleeding risk, which is particularly important given how frequently incidental arrhythmia is now detected in older people.