Palpitations are a symptom, not a diagnosis. First assess for instability, syncope, chest pain, acute breathlessness, exertional symptoms, abnormal ECG, structural heart disease and inherited arrhythmia risk. Do not label symptoms as anxiety or benign ectopy until appropriate cardiac and systemic assessment is complete, and confirm AF by ECG before long-term AF treatment.
Ventricular tachycardia (VT) is the diagnostic emergency in palpitations. It may be haemodynamically tolerated initially, giving a false reassurance window. Syncope with palpitations makes a significant arrhythmia much more likely than palpitations alone.
Patients with structural heart disease have a substantially higher risk of sudden cardiac death from VT. 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.
Pre-excitation needs specialist assessment — same-day if symptomatic or with AF; a delta wave in a well, asymptomatic patient is not automatically an emergency. 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 — a useful clue, but the rhythm must be documented.
The rhythm-tapping manoeuvre is a quick, useful clue, but the rhythm must be documented on an ECG. Regular rapid rhythm suggests SVT/flutter; irregularly irregular strongly suggests AF.
Termination with Valsalva supports SVT. 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 (ESC 2019 SVT guideline, international — NICE NG196 covers AF, not SVT).
"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.
Perform a 12-lead ECG at the initial assessment of new or unexplained palpitations whenever feasible, with competent interpretation. 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. Perform it at the initial assessment of new or unexplained palpitations whenever feasible; a normal ECG does not exclude paroxysmal arrhythmia.
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 commonly causes sinus tachycardia and sometimes AF. 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, and is often undiagnosed in people with AF. 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 often finds arrhythmias but symptoms during the recording are less common, so symptom–rhythm correlation is 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) Correct clinically important electrolyte abnormalities before drug treatment decisions, but avoid routine potassium supplementation or a fixed target — particularly in CKD or with RAAS inhibitors or potassium-sparing drugs.
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 substantially reduces stroke risk in AF. 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.
Next steps: see Atrial fibrillation · Hyperthyroidism · Anxiety disorders · DOACs, antiplatelets and anticoagulation
The REVERT trial (2015, Lancet) demonstrated that the modified Valsalva manoeuvre is more effective than standard Valsalva — a simple first step in a stable patient; adenosine, if needed, belongs in a monitored emergency setting.
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 showed fewer strokes and less 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.
Address alcohol, obesity, BP, smoking, inactivity and suspected OSA; reduce triggers that clearly reproduce symptoms.
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.
Weight-loss studies show sustained weight loss helps maintain sinus rhythm, 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.