Check these before anything else. Palpitations are benign in most cases but can be the sole presentation of a lethal arrhythmia. Never assume benign without exclusion.
Ventricular tachycardia (VT) is the diagnostic emergency in palpitations. It may be haemodynamically tolerated initially, giving a false reassurance window. Syncope with palpitations has a high probability of VT (~30% of cases) versus <5% for palpitations alone.
Patients with structural heart disease have a 10× higher risk of sudden cardiac death from VT than the general population. Missing familial channelopathies (LQTS, Brugada, ARVC) is a common cause of preventable sudden cardiac death in young adults — these require specialist ECG interpretation and genetic counselling, not GP management alone.
WPW (pre-excitation) is a NICE-cited reason for urgent same-day assessment: AV nodal blocking drugs (verapamil, digoxin, adenosine) can cause VF in AF with WPW by accelerating accessory pathway conduction.
A structured history identifies the likely mechanism and guides investigation. Ask the patient to tap out the rhythm — this single manoeuvre is highly discriminating.
The rhythm-tapping manoeuvre correctly identifies AF versus regular tachycardia with ~75% accuracy in GP studies — it costs zero and takes 30 seconds. Regular rapid rhythm suggests SVT/flutter; irregularly irregular strongly suggests AF.
Valsalva termination is near-pathognomonic for SVT (sensitivity ~80%). If a patient describes terminating attacks by breath-holding, bearing down, or cold water, they likely have AVNRT or AVRT — these patients should all be referred for electrophysiology study consideration (NICE NG196).
"Holiday heart" — AF precipitated by binge alcohol — is a distinct and common presentation in otherwise healthy 30–50 year olds. First-episode AF in this context has a high spontaneous cardioversion rate but warrants full assessment including echo and stroke risk stratification.
A 12-lead ECG is mandatory for ALL patients presenting with palpitations. Even if in sinus rhythm, look for underlying pathology that predisposes to arrhythmia.
A 12-lead ECG takes 3 minutes and costs nothing but provides irreplaceable diagnostic information. It remains the single most important investigation in palpitations. NICE CKS explicitly states it should be performed in all cases, even when the history suggests benign cause.
Broad complex tachycardia must be treated as VT until cardiology confirms otherwise — even if the patient appears haemodynamically stable. Misdiagnosis of VT as SVT with aberrancy and treating with verapamil has caused preventable cardiac arrests. The Brugada criteria (morphology rules) can help distinguish, but are best used by cardiologists or with senior input.
WPW on ECG is an RCGP SCA exam favourite. The key teaching point: patients with WPW who develop AF are at risk of VF because the accessory pathway bypasses the AV node and can conduct extremely rapidly. AV nodal blocking drugs are therefore contraindicated and the patient needs electrophysiology review for ablation consideration.
Examination rarely makes the diagnosis in palpitations but identifies precipitating conditions (anaemia, thyrotoxicosis, valve disease) and guides urgency.
Valvular heart disease is a significant precipitant of AF — AF occurs in ~30% of patients with mitral stenosis. A murmur found during palpitation workup should always prompt echocardiography before attributing symptoms to a "benign" cause.
Thyrotoxicosis causes AF in 2–5% of cases and sinus tachycardia in the majority. TFTs should be checked in all new AF presentations (NICE NG196 recommendation). Treating the arrhythmia without addressing the thyroid cause leads to treatment failure and risk of thyroid storm.
OSA is an increasingly recognised driver of AF, with epidemiological data suggesting 30–50% of AF patients have undiagnosed OSA. CPAP therapy reduces AF recurrence after cardioversion — making OSA identification a modifiable risk factor worth pursuing.
Investigate to confirm arrhythmia type, identify reversible causes, and assess cardiac function. Match investigation intensity to clinical risk.
The core challenge in palpitation investigation is that most patients present in sinus rhythm. The goal is symptom-rhythm correlation — capturing the ECG at the moment of symptoms. Without this, management remains empirical.
Holter monitoring detects an arrhythmia in ~35% of palpitation patients, but only ~13% have symptoms during the recording period, making symptom-rhythm correlation possible in a minority. This is why extending monitoring to 7 days or 28 days significantly improves diagnostic yield — particularly for paroxysmal AF, which may be asymptomatic between episodes.
Hypokalaemia potentiates virtually all arrhythmias (ectopics, AF, VT) and is entirely reversible with supplementation. Electrolyte correction should precede drug treatment decisions — many perceived "resistant" arrhythmias resolve once K⁺ >4.0 mmol/L.
Stratify by urgency. Most patients with benign ectopics can be managed in primary care. Confirmed arrhythmias and high-risk features require specialist input.
SVT ablation has a first-attempt success rate of 90–95% for AVNRT (the commonest SVT) with <1% serious complication rate. It is curative. Patients with symptomatic SVT should be counselled that ablation is an option and referred for electrophysiology review — long-term antiarrhythmic drugs are increasingly being avoided in favour of definitive ablation.
Anticoagulation in AF reduces stroke risk by 64% (absolute risk reduction ~2.7% per year in high-risk patients). The decision to anticoagulate is time-sensitive — starting in primary care while awaiting cardiology is appropriate and recommended by NICE NG196. Delaying anticoagulation pending specialist review leaves patients at preventable stroke risk.
WPW is estimated to affect 1–3 per 1000 people and carries a ~1 in 1000 per year risk of sudden death if untreated. All patients with WPW on ECG should be referred regardless of symptoms, as asymptomatic WPW can have a high-risk accessory pathway identified on electrophysiology testing that warrants ablation.
Treatment depends entirely on confirmed arrhythmia type. Treat reversible causes first. Do not start antiarrhythmic drugs empirically in unconfirmed palpitations.
The REVERT trial (2015, Lancet) demonstrated that the modified Valsalva manoeuvre converts SVT to sinus rhythm in 43% of patients, compared to 17% for standard Valsalva. This is a simple, safe, effective intervention every GP should know — it eliminates the need for IV adenosine in nearly half of SVT presentations.
DOACs are now preferred over warfarin for stroke prevention in non-valvular AF (NICE NG196). Apixaban has the strongest evidence for combined efficacy and safety — ARISTOTLE trial showed 21% relative risk reduction in stroke vs warfarin with 31% reduction in major bleeding. Rivaroxaban, edoxaban, and dabigatran are acceptable alternatives based on patient-specific factors.
Flecainide, sotalol, and amiodarone are class I/III antiarrhythmics that must only be initiated by cardiology. Flecainide causes pro-arrhythmia in structural heart disease (post-MI, reduced EF) — the CAST trial showed increased mortality. These drugs must never be started empirically in primary care without confirmed arrhythmia type and echo to exclude structural disease.
Lifestyle modification is first-line treatment for benign palpitations and adjunct therapy for AF and SVT. Frame these as effective treatments, not optional extras.
The LEGACY study (2015, JACC) was landmark evidence that intensive risk factor modification (weight loss, hypertension control, alcohol cessation, exercise) reduced AF symptom burden as effectively as antiarrhythmic drugs in overweight patients. Lifestyle modification is not an adjunct — in many patients it is the primary treatment.
The Adelaide trial demonstrated that patients who lost ≥10% of body weight had a 6× greater probability of remaining in sinus rhythm than those who did not, independent of antiarrhythmic therapy. This is data every GP managing AF patients should know and cite to motivate patients.
A trigger diary helps patients feel engaged in their own care and provides clinical data that 24-hour Holter monitoring alone cannot capture — the context of symptoms. Many patients discover their palpitations are reliably triggered by specific foods, drinks, or stressors and can be managed entirely by avoidance, without medication.
Clear safety-netting is essential — palpitations often recur and arrhythmias can progress. Ensure every patient knows the specific symptoms that require immediate action.
CHA₂DS₂-VASc scores change as patients age or acquire new comorbidities. An annual score reassessment is required — a patient who scored 1 last year may score 2 this year due to a new diagnosis of hypertension or having turned 65. Failure to do this is a common audit finding and medicolegal vulnerability in AF management.
Digoxin toxicity is a preventable drug harm — the therapeutic window is narrow and toxicity is precipitated by hypokalaemia (from concurrent diuretics), renal impairment, and drug interactions (amiodarone, clarithromycin double digoxin levels). Symptoms of toxicity include nausea, visual disturbance (yellow-green halos), bradycardia, and new arrhythmias — patients must be counselled specifically on these.
DVLA notification is a medicolegal requirement that GPs frequently miss in palpitation management. Patients with syncope or near-syncope related to arrhythmia must be advised in writing to stop driving — document this conversation clearly in the notes. Group 2 licence holders (HGV/bus drivers) have stricter standards and require specialist sign-off before returning to driving.