Palpitations
Palpitations are the subjective awareness of one's own heartbeat, often perceived as rapid, irregular, or forceful cardiac contractions.
Palpitations are defined as the unexpected awareness of one's own heartbeat [1][2]. The term comes from the Latin palpitare — "to throb, to flutter." Normally, we are blissfully unaware of our hearts beating; palpitations represent a break in that unawareness. Patients may describe them variably as "racing," "pounding," "fluttering," "skipping," or a sense of the heart "stopping."
The term itself is deliberately vague — it is a symptom, not a diagnosis. That's why it's so important to get patients to clarify what they mean and, ideally, ask the patient to tap out on the desk the rhythm and rate of the heartbeat experienced during the 'attack' [3]. This single bedside manoeuvre can transform a nebulous complaint into a working diagnosis.
Key Concept
Palpitations ≠ arrhythmia. Palpitations are a subjective symptom. Many arrhythmias (e.g., AF) are completely asymptomatic, and many patients with palpitations have no arrhythmia at all — just heightened awareness of a normal or hyperdynamic heartbeat.
Epidemiology
- Palpitations are one of the most common cardiovascular complaints in primary care, accounting for approximately 16% of general practice presentations and the second most common reason for cardiology referral (after chest pain) [4].
- Population surveys suggest lifetime prevalence of palpitations in the general population is as high as 25–35%.
- Female predominance: Women present with palpitations more frequently, partly due to higher prevalence of anxiety disorders, SVT (especially AVNRT which has F > M predominance), and hormonal fluctuations (menstrual cycle, pregnancy, menopause).
- Age distribution: Bimodal — younger patients tend to have benign causes (anxiety, ectopics, SVT, congenital syndromes), whereas older patients are more likely to have structural heart disease and atrial fibrillation.
- The vast majority of palpitations are benign — only about 10–15% turn out to be due to a cardiac arrhythmia requiring treatment.
- However, palpitations associated with syncope, structural heart disease, or ventricular arrhythmias carry significant mortality risk and must not be missed.
Risk factors for palpitations mirror the risk factors for their underlying causes:
| Category | Specific Risk Factors | Mechanism |
|---|---|---|
| Cardiac | Structural heart disease (IHD, valvular, cardiomyopathy), prior cardiac surgery, congenital heart disease | Substrate for arrhythmias (re-entry circuits, automaticity foci) |
| Drugs/Substances | Caffeine, cocaine, marijuana, alcohol [3], sympathomimetics (salbutamol, pseudoephedrine), β-blockers (withdrawal), antipsychotics, antidepressants (TCAs), thyroxine, digoxin, nifedipine [3] | Stimulate catecholamine release, prolong QT, alter automaticity |
| Electrolyte | Hypokalaemia, hypomagnesaemia [3] | Alter resting membrane potential → triggered activity, re-entry |
| Endocrine | Hyperthyroidism, phaeochromocytoma, hypoglycaemia (type 1 diabetes) [3] | ↑Sympathetic drive, ↑Na⁺/K⁺-ATPase activity |
| Lifestyle | Smoking, excessive exercise, sleep deprivation | ↑Catecholamines, vagal withdrawal |
| Psychological | Anxiety, depression, panic disorder [3] | ↑Sympathetic tone + heightened interoception (awareness of body signals) |
| Physiological | Pregnancy, menopause, fever/infection [3] | Hyperdynamic circulation (↑blood volume, ↑HR, ↓SVR) |
| Genetic | Family history of sudden cardiac death, Long QT syndrome, Wolff–Parkinson–White (WPW) syndrome [3] | Inherited channelopathies or accessory pathways |
| Haematological | Anaemia [3] | Compensatory ↑HR and ↑stroke volume → hyperdynamic state |
Anatomy and Physiology of the Cardiac Conduction System
To understand why palpitations occur, you need to understand the normal electrical conduction of the heart — because palpitations ultimately arise from disturbances in this system, or from the heart beating normally but being perceived abnormally.
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SA node (sinoatrial node): Located at the junction of the SVC and right atrium. It is the heart's natural pacemaker, firing at an intrinsic rate of 60–100 bpm. It is richly innervated by both sympathetic (↑rate) and parasympathetic/vagal (↓rate) fibres.
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Atrial conduction: Impulse spreads through atrial myocardium → atrial contraction (P wave on ECG).
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AV node (atrioventricular node): Sits in the Triangle of Koch (between coronary sinus, tricuspid valve, and tendon of Todaro). It is the only normal electrical connection between atria and ventricles. It introduces a deliberate delay (~120ms) to allow atrial contraction to fill the ventricles before ventricular systole. This is the basis of the PR interval.
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His-Purkinje system: Bundle of His → left and right bundle branches → Purkinje fibres → ventricular myocardium → coordinated ventricular contraction (QRS complex).
There are three fundamental mechanisms by which abnormal rhythms arise:
| Mechanism | Description | Examples |
|---|---|---|
| Abnormal automaticity | A focus outside the SA node develops spontaneous depolarization, either by enhanced normal automaticity or by abnormal automaticity in cells that don't normally fire spontaneously | Sinus tachycardia, some atrial tachycardias, accelerated idioventricular rhythm |
| Re-entry | An electrical impulse travels in a circuit repeatedly, re-exciting tissue. Requires: (1) two pathways with different conduction velocities and refractory periods, (2) unidirectional block in one pathway, (3) slow conduction in the other | AVNRT, AVRT (WPW), atrial flutter, most VTs in structural heart disease |
| Triggered activity | Oscillations in membrane potential during or after repolarization (early or delayed afterdepolarizations) trigger premature firing | Digoxin toxicity (DADs), Long QT/Torsades de Pointes (EADs), catecholaminergic polymorphic VT |
Why does this matter clinically?
Understanding the mechanism tells you how to treat. Re-entrant tachycardias can be terminated by breaking the circuit (vagal manoeuvres, adenosine, ablation). Automatic tachycardias cannot be cardioverted — they just restart. Triggered activity is managed by removing the trigger (correcting electrolytes, stopping offending drugs).
Aetiology
This is the core of the clinical approach. The causes of palpitations fall into three broad pathophysiological categories [1][2]:
Palpitations can result from: (1) Tachyarrhythmias felt by patients, (2) Hyperdynamic circulation exaggerating sinus rhythm, (3) Bradyarrhythmias with strong beats (↑diastolic time → ↑stroke volume) [1][2]
Category 1: Tachyarrhythmias
These are the primary cardiac causes.
| Site of Origin | Tachyarrhythmias | Bradyarrhythmias |
|---|---|---|
| SA node | Sinus tachycardia (ST) | Sinus bradycardia, Sick sinus syndrome, Sinus arrest, Sinoatrial block |
| Atrial muscle | Atrial tachycardia (AT), Atrial flutter (AFL), Atrial fibrillation (AF), Atrial premature beats/ectopics (APB) | Atrial escape |
| AV node | AV re-entrant tachycardia (AVRT), AV nodal re-entrant tachycardia (AVNRT), Junctional tachycardia | AV blocks, Junctional escape |
| Ventricles | Ventricular tachycardia (VT), Ventricular fibrillation (VF), Ventricular premature beats/ectopics (VPB) | Ventricular escape |
Sinus tachycardia (ST)
- Most common cause of a fast, regular palpitation
- Not a primary arrhythmia — it is the appropriate response to a physiological or pathological stimulus
- Causes: exercise, fever, anxiety, pain, anaemia, thyrotoxicosis, dehydration, drugs (sympathomimetics, caffeine), heart failure, PE
- Pathophysiology: ↑sympathetic drive or ↓vagal tone → ↑SA node firing rate
- Rate: 100–180 bpm, regular, gradual onset and offset
Premature beats (ectopics) — atrial and ventricular [3]
- The single most common cause of palpitations in clinical practice
- Atrial premature beats (APB): premature depolarisation originating from ectopic atrial focus
- Ventricular premature beats (VPB): premature depolarisation originating from ventricular focus
- Why patients feel them: the premature beat itself is often too weak to generate a good pulse (under-filled ventricle), but the compensatory pause that follows allows extra diastolic filling → the next normal beat is unusually forceful → patient perceives a "thump" or "skip"
- Common triggers: smoking, anxiety and excessive caffeine [3], alcohol, nicotine, worse at rest [1][2]
Supraventricular tachycardia (SVT) [3] — a broad term encompassing:
AVNRT (AV Nodal Re-entrant Tachycardia)
- Young patients, F > M [1][2]
- Most common paroxysmal SVT
- Mechanism: re-entry within or near the AV node — the AV node has two functional pathways (fast and slow); the circuit goes down one and up the other
- Sudden onset, sudden termination [1][2]
- Terminated by vagal manoeuvres (e.g., sneeze, cough, defecation) [1][2] — because the AV node is the vulnerable link in the circuit; increased vagal tone slows AV nodal conduction and breaks the circuit
- Rate: 150–250 bpm, very regular
AVRT (AV Re-entrant Tachycardia)
- Involves an accessory pathway (e.g., Wolff–Parkinson–White (WPW) syndrome [3])
- WPW → "W" = wide on ECG when pre-excited, "P" = pathway (Bundle of Kent), "W" = Wolff
- Mechanism: macro-re-entry circuit using the AV node as one limb and the accessory pathway as the other
- Sudden onset and termination [1][2], also responsive to vagal manoeuvres
- Danger: if AF develops in WPW, the accessory pathway can conduct very rapidly → VF → sudden cardiac death
Atrial fibrillation (AF) [3]
- The most common sustained arrhythmia globally
- Very relevant in Hong Kong's ageing population
- Mechanism: multiple chaotic re-entrant wavelets in the atria → completely disorganized atrial activity → irregularly irregular ventricular response
- Pathophysiology: structural remodelling (atrial dilatation, fibrosis) → heterogeneous conduction → perpetuates AF ("AF begets AF")
- Risk factors: age, hypertension, HF, valvular disease (esp mitral stenosis), thyrotoxicosis, alcohol ("holiday heart"), obesity, OSA
- Irregular palpitations → think AF [1][2]
Atrial flutter (AFL) [3]
- Mechanism: macro-re-entrant circuit in the right atrium, typically around the tricuspid valve annulus (cavotricuspid isthmus-dependent)
- Atrial rate ~300 bpm with typical 2:1 AV block → ventricular rate ~150 bpm (regular)
- AFL/AT with variable block can mimic AF with irregular palpitations [1][2]
Atrial tachycardia (AT)
- Mechanism: abnormal automaticity, re-entry at single atrial focus (microreentry), triggered activity [5]
- Causes: no underlying disease (good prognosis), atrial enlargement, digitalis toxicity [5]
- Atrial rate 110–250 bpm, abnormal P-wave morphology
Multifocal atrial tachycardia (MAT)
Ventricular tachycardia (VT) [3]
- ≥3 consecutive ventricular beats at >100 bpm
- Most commonly associated with structural heart disease (prior MI with scar → re-entrant circuit)
- Dangerous — can degenerate into VF → cardiac arrest
- May present as palpitations, syncope, or sudden death
- During exercise: think PSVT, AF and VT [1][2]
Ventricular fibrillation (VF) [3]
- Chaotic, uncoordinated ventricular activity → no effective cardiac output → cardiac arrest
- Patient will not be conscious to report palpitations — but VF often preceded by VT, which may cause preceding palpitations
Torsades de Pointes (TdP) [3]
- A specific form of polymorphic VT occurring in the setting of prolonged QT interval
- "Torsades de Pointes" = French for "twisting of the points" — the QRS complexes twist around the isoelectric line
- Causes: drugs (antiarrhythmics, antipsychotics, macrolides, fluoroquinolones), hypokalaemia, hypomagnesaemia [3], congenital Long QT syndrome [3]
These cause palpitations by exaggerating sinus rhythm — the heart beats normally but harder/faster, and the patient becomes aware of it.
Regular, relatively fast pounding (90–120 bpm) → think hyperdynamic circulation (anaemia, pregnancy, thyrotoxicosis, AR, PDA) [1][2]
| Cause | Mechanism of Hyperdynamic State |
|---|---|
| Anaemia [3] | ↓O₂ carrying capacity → compensatory ↑HR + ↑SV to maintain O₂ delivery |
| Pregnancy [3] | ↑Blood volume by 40–50%, ↓SVR (progesterone effect), ↑CO |
| Thyrotoxicosis [3] | T4 ↑β-adrenergic receptor expression, ↑Na⁺/K⁺-ATPase activity, ↑cardiac contractility, ↓SVR |
| Fever/infection [3] | Metabolic demands ↑ → sympathetic activation → ↑HR (~10 bpm per 1°C) |
| Aortic regurgitation (AR) | Wide pulse pressure → forceful LV ejection → patient feels the "water-hammer" pulse |
| PDA (Patent Ductus Arteriosus) | Left-to-right shunt → volume overload of left heart → ↑SV |
| Menopause [3] | Oestrogen withdrawal → vasomotor instability, sympathetic activation |
| Exercise [3] | ↑Sympathetic drive → ↑HR and contractility |
Anxiety [3] — the single most common cause in Murtagh's "probability diagnosis"
- Anxiety and cardiac neurosis [3] are extremely common causes of palpitations
- Mechanism: ↑sympathetic activation → sinus tachycardia + heightened interoceptive awareness (the brain's threat-detection system amplifies perception of normal heartbeat)
- Depression [3] (masquerade checklist): often coexists with anxiety; SSRIs and TCAs can themselves cause palpitations
Panic disorder [6]:
- Recurrent, unexpected panic attacks with intense autonomic symptoms including palpitations, chest pain, SOB, diaphoresis, tremor
- Patients genuinely believe they are having a heart attack
- ↑Anxiety sensitivity: fear of anxiety symptoms and catastrophic cognition regarding bodily sensations (e.g., misattribution of rapid heartbeat as heart attack) [6]
Somatoform disorder [7]:
- CVS/resp symptoms including chest pain, SOB, palpitations are common somatic presentations [7]
- Excessive health-seeking behaviour, high utilization
Drugs deserve special emphasis as a cause [3]:
| Drug Category | Examples | Mechanism |
|---|---|---|
| Stimulants [3] | Caffeine, cocaine, amphetamines, MDMA | ↑Catecholamine release → ↑automaticity, trigger ectopics/SVT |
| Prescribed drugs [3] | β-blockers (rebound tachycardia on withdrawal), antipsychotics (QT prolongation), antidepressants (TCAs) (anticholinergic + Na⁺ channel blockade), thyroxine (iatrogenic thyrotoxicosis), digoxin (toxicity → multiple arrhythmias), nifedipine (reflex tachycardia from vasodilation), sympathomimetics (salbutamol, adrenaline) | Various — see individual mechanisms |
| Alcohol [3] | Acute binge ("holiday heart") or chronic | Direct myocardial toxicity + electrolyte derangement (↓K⁺, ↓Mg²⁺) → AF, atrial flutter |
| Marijuana [3] | THC | ↑Sympathetic tone, ↓parasympathetic → sinus tachycardia |
This is from the lecture slides — extremely high yield:
Probability diagnosis: Anxiety, Premature beats (ectopics) — atrial and ventricular, Sinus tachycardia (e.g., fever, exercise), Supraventricular tachycardia, Drugs (e.g., stimulants) [3]
Serious disorders not to be missed: Myocardial infarction/angina, Arrhythmias (atrial fibrillation or flutter, ventricular tachycardia, bradycardia/heart block, sick sinus syndrome, torsade de pointes), Long QT syndrome, Wolff–Parkinson–White (WPW) syndrome, Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypoglycaemia in type 1 diabetes) [3]
Pitfalls (often missed): Fever/infection, Pregnancy, Menopause, Drugs (e.g., caffeine, cocaine), Mitral valve disease, Aortic incompetence, Hypoxia/hypercapnia [3]
Rarities: Tick bites (T1–5), Phaeochromocytoma [3]
Masquerades checklist: Depression, Diabetes (indirect), Drugs (see list), Anaemia, Thyroid disorder (hyperthyroidism), Spinal dysfunction [3]
Is the patient trying to tell me something? Quite likely. Consider cardiac neurosis, anxiety. [3]
Classification
- Primary arrhythmic — the heart's electrical system is genuinely misbehaving
- Secondary to systemic cause — heart is responding appropriately to an abnormal milieu (e.g., sinus tachycardia in anaemia)
- Non-cardiac/functional — heightened perception of normal or near-normal heart activity (e.g., anxiety, somatization)
- Benign/no haemodynamic compromise: most ectopics, sinus tachycardia, anxiety
- Potentially life-threatening: sustained VT, VF, TdP, WPW with AF, severe bradycardia
- Paroxysmal: discrete episodes with clear start/stop (e.g., AVNRT, paroxysmal AF)
- Persistent: ongoing (e.g., persistent AF, incessant AT)
- Chronic/permanent: established permanent AF
- Tachyarrhythmias ( > 100 bpm)
- Bradyarrhythmias ( < 60 bpm)
- Normal rate (hyperdynamic/functional)
Clinical Features
The clinical approach to palpitations centres on a meticulous history — this is a history-driven diagnosis. By the time you examine the patient, the palpitations have usually stopped, and the examination is often normal.
The ideal time to examine the patient is during the palpitations. If not, the examination is usually normal. [3]
A. Symptoms (History)
The history is structured around specific features that narrow the differential:
Ask the patient to describe the onset and offset of the palpitations, the duration of each episode and any associated features. Then ask the patient to tap out on the desk the rhythm and rate of the heartbeat experienced during the 'attack'. If the patient is unable to do this, tap out the cadence of the various arrhythmias to find a matching beat. [3]
| Description | Most Likely Cause | Pathophysiological Basis |
|---|---|---|
| Skipped or 'heavy' beats [1][2] | Ectopic beats (APB or VPB) | The premature beat under-fills the ventricle → weak/absent pulse, but the compensatory pause allows extra filling → next beat is hyperdynamic → patient feels a "thump" followed by a "skip" |
| An isolated thump or jump followed by a definite pause on a background of a regular pattern [3] | Premature beats (ectopics), usually ventricular [3] | Same mechanism as above |
| Irregular palpitations ('all over the place') [1][2][3] | AF, AFL/AT with variable block, MFAT | Chaotic atrial activity → irregular ventricular response → irregular pulse perceived as "fluttering" or "all over the place" |
| Regular, relatively fast pounding (90–120 bpm) [1][2] | Hyperdynamic circulation (anaemia, pregnancy, thyrotoxicosis, AR, PDA) | ↑Stroke volume and/or ↑heart rate in the setting of high-output states → forceful, regular beats |
| Discrete bouts, very rapid ( > 120 bpm) [1][2] | Paroxysmal nodal re-entrant tachycardia | Re-entrant circuit fires at very high rate → sudden onset of rapid, regular pounding |
| Slow, heavy beating | Bradycardia (sinus, heart block) | ↑Diastolic filling time → ↑stroke volume → each beat felt more forcefully |
| Fluttering in the chest | SVT, AF, anxiety | Rapid rate or irregular rhythm perceived as a "flutter" |
| Feature | Interpretation | Mechanism |
|---|---|---|
| Insidious onset/offset [1][2] | ↑Automaticity → sinus tachycardia, some AT | SA node gradually increases its firing rate in response to sympathetic tone |
| Sudden onset/offset [1][2] | Re-entrant circuit → AVRT, AVNRT, some AT | Re-entry is an all-or-nothing phenomenon — circuit either sustains or collapses |
| Arrhythmia of sudden onset [3] | Suggests PSVT, atrial flutter/fibrillation or ventricular tachycardia [3] | Re-entry or triggered activity — abrupt initiation |
| Trigger | Most Likely Cause | Mechanism |
|---|---|---|
| At rest [1][2] | Ectopics and AF | ↑Vagal tone at rest → shortens atrial refractory period → facilitates re-entry in AF; ectopics are more noticeable when resting (low background sympathetic "noise") |
| During exercise [1][2] | PSVT, AF, VT | ↑Catecholamines → ↑automaticity and conduction velocity → can initiate re-entry or trigger ectopics that induce SVT; exercise-induced VT suggests structural heart disease or CPVT |
| Stress, emotional upset | Anxiety, sinus tachycardia, ectopics | ↑Sympathetic → ↑HR + heightened awareness |
| Postprandial / after carbohydrate load | Thyrotoxic periodic paralysis (palpitation component) [8] | ↑Insulin → ↑Na⁺/K⁺-ATPase → hypoK → arrhythmia risk |
| Alcohol binge | AF ("holiday heart"), ectopics | Direct atrial myocardial toxicity + ↓K⁺/Mg²⁺ |
| Caffeine, tea, energy drinks [3] | Sinus tachycardia, ectopics, SVT | Adenosine receptor antagonism → ↑sympathetic, ↑catecholamines |
| Drugs [3] | Various (see above) | Drug-specific mechanisms |
| Positional (bending, lying on left side) | Ectopics, anxiety | Heart closer to chest wall when lying left → more easily felt; also vagal changes with position |
| Feature | Interpretation | Mechanism |
|---|---|---|
| Terminated by vagal manoeuvres (e.g., sneeze, cough, defecation) [1][2] | Nodal re-entrant tachycardia (AVNRT/AVRT) | ↑Vagal tone → slows/blocks conduction through AV node → breaks the re-entrant circuit that depends on AV nodal conduction |
| Gradual offset | Sinus tachycardia, AT due to automaticity | Gradual ↓sympathetic drive → gradual slowing |
| Abrupt offset without vagal manoeuvre | Re-entrant SVT, paroxysmal AF | Circuit spontaneously terminates |
Young: think congenital syndromes (e.g., LQTS, WPWS), AVNRT [1][2] Older: think other arrhythmias esp those a/w underlying structural heart disease [1][2]
- Young patients: congenital accessory pathways (WPW), inherited channelopathies (Long QT, Brugada, CPVT), AVNRT (most common SVT in young women)
- Older patients: AF (prevalence rises sharply with age), VT from ischaemic scar, sick sinus syndrome
These help determine haemodynamic significance and underlying cause:
| Associated Symptom | Suggests | Mechanism |
|---|---|---|
| Syncope / presyncope | VT, severe bradycardia, LVOT obstruction (HCMP), massive PE | ↓CO → ↓cerebral perfusion |
| Chest pain | ACS, HCMP, severe tachycardia causing supply-demand mismatch | ↑HR → ↓diastolic filling time → ↓coronary perfusion + ↑myocardial O₂ demand |
| Dyspnoea | Heart failure, PE, anaemia, anxiety | Pulmonary congestion (HF), ↓O₂ delivery (anaemia), hyperventilation (anxiety) |
| Polyuria post-attack | SVT (especially AVNRT) | Atrial distension during tachycardia → release of atrial natriuretic peptide (ANP) → diuresis |
| Diaphoresis | VT, MI, phaeochromocytoma, hypoglycaemia, panic | Sympathetic activation |
| Weight loss, heat intolerance, tremor | Thyrotoxicosis | ↑Metabolic rate from excess T3/T4 |
| Anxiety, hyperventilation, paraesthesia | Panic disorder, anxiety | Hyperventilation → respiratory alkalosis → ↓ionized Ca²⁺ → peripheral paraesthesia |
Take a past history and family history including caffeine intake, smoking, alcohol, social drugs such as marijuana or cocaine, and prescribed drugs (β-blockers, antipsychotics, antidepressants, thyroxine, digoxin, nifedipine, sympathomimetics) [3]
- Prior structural heart disease (IHD, valvular, cardiomyopathy) — substrate for arrhythmia
- Thyroid disease
- Psychiatric history (anxiety, panic disorder, depression)
- Family history: sudden cardiac death (especially < 40 years), cardiomyopathy, Long QT, WPW
Red Flag Features in Palpitation History
The following features suggest a serious/life-threatening cause and demand urgent evaluation:
- Syncope or near-syncope during palpitations
- Palpitations during exercise (especially if associated with chest pain or syncope)
- Family history of sudden cardiac death ( < 40 years)
- Known structural heart disease
- Very rapid rate ( > 150 bpm) or very slow rate
- Associated chest pain or dyspnoea
- Abnormal baseline ECG
B. Signs (Examination)
The cardiovascular examination should assess the pulse rate, rhythm, volume and character [3] The general examination should investigate features suggestive of anaemia, anxiety, tremors, dyspnoea and thyroid disease [3] Look for evidence of mitral valve prolapse [3]
| Sign | What It Suggests | Pathophysiological Basis |
|---|---|---|
| Irregularly irregular pulse | AF | No organized atrial contraction → variable RR intervals |
| Regular rapid pulse ( > 150 bpm) | SVT, atrial flutter with fixed block, VT | Re-entrant or automatic tachycardia at high rate |
| Bradycardia ( < 60 bpm) | Sinus bradycardia, heart block | ↓SA node automaticity or AV conduction block |
| Collapsing (water-hammer) pulse | Aortic regurgitation | Wide pulse pressure from large SV + rapid diastolic runoff |
| Displaced, hyperdynamic apex | LV dilatation (DCMP, AR, volume overload) | Enlarged LV shifts apex laterally and inferiorly |
| Mid-systolic click ± late systolic murmur | Mitral valve prolapse [3] | Myxomatous degeneration → prolapse of leaflet → click from sudden tensing of chordae, murmur from MR |
| Mid-diastolic rumbling murmur (at apex) | Mitral stenosis (think AF as common sequela) | Turbulent flow across stenotic mitral valve; MS is the classic substrate for AF due to left atrial dilatation |
| Ejection systolic murmur (LLSE, varies with manoeuvres) | HCMP | Dynamic LVOT obstruction worsens with ↓preload (e.g., standing, Valsalva) |
| S3 gallop | Heart failure, volume overload | Rapid ventricular filling in a dilated, non-compliant ventricle |
| Elevated JVP with cannon A waves | Complete heart block, VT | Atria contracting against closed AV valves (A-V dissociation) |
| Elevated JVP with irregular cannon A waves | AF (no organized atrial contraction) | Variable atrial contraction timing relative to ventricular systole |
| Sign | What It Suggests | Mechanism |
|---|---|---|
| Pallor (conjunctival/palmar crease) | Anaemia → hyperdynamic palpitations | ↓Haemoglobin → ↓O₂ delivery → compensatory ↑CO |
| Tremor (fine resting tremor of hands) | Thyrotoxicosis, anxiety | ↑β-adrenergic stimulation of skeletal muscle |
| Thyroid enlargement (goitre) ± bruit | Graves' disease | ↑TSH receptor stimulation by TRAb → gland hyperplasia + ↑vascularity |
| Lid lag / lid retraction | Thyrotoxicosis (non-specific sign) | ↑Sympathetic tone → overactive Müller's muscle (smooth muscle in eyelid) |
| Exophthalmos | Graves' ophthalmopathy (specific to Graves') | Autoimmune infiltration of orbital fat and extraocular muscles |
| Xanthomata / arcus / obesity | Cardiovascular risk factors | Dyslipidaemia, metabolic syndrome |
| Café-au-lait spots, neurofibromas | NF1 → consider phaeochromocytoma | NF1 mutation → predisposition to chromaffin cell tumours |
| Marfanoid habitus | MVP, aortic root dilatation → AR | Fibrillin-1 defect → connective tissue disorder affecting heart valves |
| Anxiety features: hyperventilation, sweating, agitation | Panic disorder, GAD | Sympathetic activation + cognitive amplification |
Pathophysiology of Specific Important Aetiologies (Hong Kong Focus)
- Prevalence in HK: ~1.3% overall, rising to > 10% in > 80 years
- The "AF substrate" develops through:
- Atrial dilatation (from hypertension, HF, valvular disease) → stretching of atrial myocytes → altered gap junction distribution
- Atrial fibrosis → slow, heterogeneous conduction → multiple simultaneous re-entry wavelets
- Electrical remodelling: AF itself shortens atrial refractory periods → "AF begets AF"
- Pulmonary vein triggers: ectopic foci in the pulmonary vein ostia can trigger AF (basis for PV isolation ablation)
- In Hong Kong, rheumatic heart disease (esp mitral stenosis) remains a cause of AF in older patients, though hypertensive heart disease is now the dominant substrate
- Up to 2% among Asian patients with hyperthyroidism [8]
- Usu in young Asian male [8]
- Classic triad of hyperthyroidism + hypoK + paralysis; cardiac arrhythmia due to severe hypoK (mean serum [K] = 2.1) [8]
- Palpitations occur both from thyrotoxicosis itself (sinus tachycardia, AF) and from hypoK-mediated arrhythmias
- Classic triad: paroxysmal headache + sweating + palpitations ( > 90% predictive) [9][10]
- Palpitations (70%) [9]
- 5 P's: Pressure (HT), Pain (headache, chest pain), Palpitation, Perspiration, Pallor (vasoconstriction) [10]
- Mechanism: episodic catecholamine surges → ↑HR, ↑contractility, ↑BP → patient acutely aware of pounding heart
- Palpitations and arrhythmias (both VT and SVT esp AF) [11]
- HCMP is the most common cause of sudden cardiac death in young athletes
- Palpitations in HCMP can be from: AF (30% of patients), non-sustained VT, VPBs, or the dynamic LVOT obstruction causing a hyperdynamic but inefficient cardiac output
- Apical HCMP: 25–30% of HCMP in Japan and HK [12] — presents with palpitation, chest pain, diastolic HF
High Yield Summary
-
Definition: Palpitations = unexpected awareness of heartbeat. It is a symptom, not a diagnosis.
-
Three mechanisms: (a) Tachyarrhythmias, (b) Hyperdynamic circulation exaggerating sinus rhythm, (c) Bradyarrhythmias with strong beats (↑diastolic filling → ↑stroke volume).
-
Probability diagnosis (Murtagh): Anxiety, ectopics, sinus tachycardia, SVT, drugs/stimulants.
-
Must not miss: MI, AF/AFL, VT, bradycardia/heart block, sick sinus syndrome, TdP, Long QT, WPW, hypoK/hypoMg, hypoglycaemia.
-
Pitfalls often missed: Fever, pregnancy, menopause, caffeine/cocaine, mitral valve disease, AR, hypoxia.
-
Masquerades: Depression, diabetes, drugs, anaemia, thyrotoxicosis, spinal dysfunction.
-
Key history features: Character (tap it out!), onset/offset (sudden = re-entry, gradual = automaticity), triggers, termination (vagal manoeuvres = nodal re-entry), age, associated symptoms (syncope = red flag), drug/substance use, family history of SCD.
-
Key examination: Usually normal between attacks. Check pulse (rate, rhythm, volume, character), look for anaemia, thyroid disease, anxiety, MVP, structural heart disease signs.
-
HK-relevant aetiologies: AF (ageing population), TPP (young Asian males), HCMP (esp apical variant 25-30% in HK/Japan), phaeochromocytoma (5P's).
-
Red flags: Syncope, exertional palpitations, FHx of SCD, structural heart disease, chest pain, abnormal ECG.
Active Recall - Palpitations (Definition, Epidemiology, Aetiology, Clinical Features)
[1] Senior notes: Ryan Ho Cardiology.pdf (p61, Section 2.3 Palpitations) [2] Senior notes: Ryan Ho Fundamentals.pdf (p206, Section 3.1.3 Palpitations) [3] Lecture slides: murtagh merge.pdf (p72–74, Palpitations) [4] General medical knowledge — prevalence data from UpToDate / Harrison's Principles of Internal Medicine [5] Senior notes: Ryan Ho Cardiology.pdf (p92, Focal and Multifocal Atrial Tachycardia) [6] Senior notes: Ryan Ho Psychiatry.pdf (p178–180, Panic Disorder) [7] Senior notes: Ryan Ho Psychiatry.pdf (p202, Somatic Symptom Disorder) [8] Senior notes: Ryan Ho Endocrine.pdf (p29, Thyrotoxic Periodic Paralysis) [9] Senior notes: Ryan Ho Endocrine.pdf (p66, Phaeochromocytoma) [10] Senior notes: maxim.md (Section on Phaeochromocytoma, 5 P's) [11] Senior notes: Ryan Ho Cardiology.pdf (p167, HCMP Clinical Features) [12] Senior notes: Ryan Ho Cardiology.pdf (p169, Apical HCMP)
Differential Diagnosis of Palpitations
The differential diagnosis of palpitations is broad precisely because the symptom itself is non-specific — it is simply the brain's awareness of the heart doing something different. Your job as a clinician is to sort through the noise and identify the signal. The framework below organises the DDx logically by mechanism, then shows you how the history, examination, and simple bedside observations allow you to narrow it down efficiently.
Recall from the previous section the three fundamental mechanisms [1][2]:
Palpitations can result from: (1) Tachyarrhythmias felt by patients, (2) Hyperdynamic circulation exaggerating sinus rhythm, (3) Bradyarrhythmias with strong beats (↑diastolic time → ↑stroke volume) [1][2]
On top of these, we must add a fourth category that is clinically crucial:
- Non-cardiac / Functional — heightened interoceptive awareness of a normal heartbeat (anxiety, panic disorder, somatoform disorders)
This gives us a practical four-box DDx model:
Complete Differential Diagnosis Table
The table below integrates Murtagh's lecture framework with the senior notes, organised by clinical likelihood.
These are what you'll see day in, day out. In a primary care or A&E setting, the vast majority of palpitation presentations fall here.
| Diagnosis | Key Distinguishing Features | Why It Causes Palpitations (Mechanism) |
|---|---|---|
| Anxiety [3] | Palpitations with hyperventilation, paraesthesia, dry mouth, tremor, sense of dread; often young patient; normal ECG; symptoms reproducible with hyperventilation | ↑Sympathetic drive → sinus tachycardia + heightened interoception. The amygdala's threat-detection system becomes hyperactive → the brain amplifies perception of a physiologically normal heartbeat [6] |
| Premature beats (ectopics) — atrial and ventricular [3] | Isolated thump or jump followed by a definite pause on a background of a regular pattern [3]; often triggered by stress, alcohol, nicotine, worse at rest [1][2] | The premature beat under-fills the ventricle → weak/absent pulse. The compensatory pause prolongs diastole → next beat has ↑stroke volume → forceful "thump." Why worse at rest? Low background sympathetic "noise" means each beat is more noticeable, plus ↑vagal tone shortens atrial refractory period facilitating ectopics |
| Sinus tachycardia, e.g. fever, exercise [3] | Regular, fast pounding with gradual onset/offset; rate 100–150 bpm; clear physiological trigger; P waves present with normal morphology before each QRS | SA node firing rate ↑ in response to sympathetic stimulation or vagal withdrawal — this is an appropriate physiological response, not a primary arrhythmia |
| Supraventricular tachycardia [3] | Discrete bouts, very rapid ( > 120 bpm) [1][2]; sudden onset and offset [1][2]; terminated by vagal manoeuvres [1][2]; polyuria post-attack (ANP release from atrial distension) | Re-entrant circuit (AVNRT/AVRT) or abnormal automaticity (AT) generates a rapid, regular supraventricular rhythm. Why sudden onset? Re-entry is all-or-nothing — the circuit either sustains or doesn't |
| Drugs (e.g. stimulants) [3] | Clear temporal relationship to drug/substance intake; caffeine, cocaine [3], β-blockers (withdrawal), antipsychotics, antidepressants, thyroxine, digoxin, nifedipine, sympathomimetics [3] | Mechanism is drug-specific: sympathomimetics ↑catecholamines → ↑automaticity; nifedipine → reflex tachycardia from vasodilation; digoxin → DAD-mediated triggered activity; antipsychotics/TCAs → QT prolongation → risk of TdP |
Clinical Priority
These are the ones that will kill your patient. Even if they're less common, you must actively exclude them in every palpitation workup.
| Diagnosis | Key Distinguishing Features | Why It Causes Palpitations | Why It's Dangerous |
|---|---|---|---|
| Myocardial infarction/angina [3] | Palpitations + chest pain (crushing, radiating to jaw/arm), diaphoresis, dyspnoea; risk factors for CAD; ECG changes (ST elevation/depression, T-wave inversion) | Myocardial ischaemia → irritable myocardium → ectopics, sinus tachycardia (sympathetic surge), VT/VF; also reflex tachycardia from ↓CO | VT/VF → cardiac arrest. CAD accounts for 85% of cardiac arrest causes [13] |
| Atrial fibrillation or flutter [3] | Irregular palpitations ('all over the place') [1][2][3]; may be paroxysmal; risk factors: age, HTN, valvular disease, thyrotoxicosis, alcohol | AF: chaotic re-entrant wavelets in atria → irregularly irregular ventricular response. AFL: macro-re-entry around tricuspid annulus → atrial rate ~300 bpm with AV block | Thromboembolism → stroke (AF ↑ stroke risk 5-fold); rapid ventricular rate → haemodynamic compromise; tachycardia-mediated cardiomyopathy |
| Ventricular tachycardia [3] | Palpitations ± syncope ± chest pain; usually exertional in structural heart disease; broad complex tachycardia on ECG; prior MI or known cardiomyopathy | Re-entry around myocardial scar (most commonly post-MI) → rapid ventricular rate with poor diastolic filling | Can degenerate to VF → cardiac arrest. Any wide complex tachycardia should be treated as VT until proven otherwise |
| Bradycardia/heart block [3] | Slow, forceful pounding; presyncope/syncope; fatigue; older patient or on rate-slowing drugs | ↑Diastolic time → ↑stroke volume → each beat felt more forcefully [1][2]; in complete heart block, cannon A waves from AV dissociation may be felt in the neck | Severe bradycardia → ↓CO → syncope → asystole |
| Sick sinus syndrome [3] | Alternating fast and slow episodes (tachy-brady syndrome [14]); syncope during the pause after tachycardia terminates; elderly | During tachyarrhythmia (usually AF), there is overdrive suppression of SA node → period of sinus arrest following termination [14] → the long pause causes syncope | Asystolic pauses → syncope, falls, cardiac arrest |
| Torsade de pointes [3] | Palpitations → syncope → may self-terminate or degenerate to VF; prolonged QTc on baseline ECG; precipitated by drugs, hypokalaemia, hypomagnesaemia [3] | "Torsades" = "twisting of the points" — polymorphic VT with QRS complexes rotating around the isoelectric line. Mechanism: prolonged repolarization → early afterdepolarizations (EADs) → triggered activity | Self-terminating → palpitations/syncope; sustained → VF → death |
| Long QT syndrome [3] | Young patient; FHx of sudden cardiac death or drowning; syncope with exercise or startle (LQT1/2) or during sleep (LQT3) | Inherited K⁺ or Na⁺ channelopathies → prolonged ventricular repolarization → EADs → TdP | Sudden cardiac death in otherwise healthy young people |
| Wolff–Parkinson–White (WPW) syndrome [3] | Young: think congenital syndromes (e.g. LQTS, WPWS) [1][2]; delta wave on resting ECG; SVT with sudden onset; risk of pre-excited AF → very rapid rate | Accessory pathway (Bundle of Kent) creates macro-re-entrant circuit with AV node. In orthodromic AVRT: AV node down, accessory pathway up → narrow complex SVT | If AF develops, the accessory pathway conducts without AV nodal delay → extremely rapid ventricular rate → VF → SCD. This is why AV nodal blockers (digoxin, verapamil) are contraindicated in pre-excited AF |
| Electrolyte disturbances: hypokalaemia, hypomagnesaemia [3] | Diuretic use, vomiting/diarrhoea, renal disease; muscle weakness, cramps; U waves on ECG (hypoK), prolonged QT | HypoK: ↑resting membrane potential → delayed repolarization → ↑QT interval → EADs → ectopics, VT, TdP. HypoMg: Mg²⁺ normally stabilises K⁺ channels; depletion → refractory hypoK + independent arrhythmogenesis | Severe hypoK ( < 2.5) → VT/VF; often coexists with hypoMg making the situation worse |
| Hypoglycaemia (type 1 diabetes) [3] | Adrenergic symptoms: palpitation, sweating, anxiety, tremor, tachycardia [15]; confirmed by low BG; in diabetics on insulin/sulfonylureas | Hypoglycaemia → counter-regulatory catecholamine surge → sinus tachycardia + ↑contractility → patient perceives forceful, rapid heartbeat; also hypoGly directly prolongs QT → risk of TdP | Neuroglycopenia → seizures, coma; prolonged QT → arrhythmia |
These are the diagnoses that catch clinicians off-guard because they're not classically associated with palpitations, or the presentation is atypical.
| Diagnosis | Why It's Missed | Mechanism of Palpitations |
|---|---|---|
| Fever/infection [3] | Palpitations attributed to the infection itself rather than recognised as a distinct symptom | Fever ↑metabolic demand → ↑sympathetic drive → sinus tachycardia (~10 bpm per 1°C). Sepsis → vasodilation → compensatory ↑HR. Some infections (myocarditis) directly damage conduction tissue |
| Pregnancy [3] | Not always disclosed or asked about; early pregnancy may not be obvious | ↑Blood volume by 40–50%, ↓SVR (progesterone), ↑CO by 30–50% → hyperdynamic circulation → sinus tachycardia felt as palpitations. The heart is also physically displaced by the gravid uterus in late pregnancy |
| Menopause [3] | Attributed to "hot flushes" rather than evaluated cardiologically | Oestrogen withdrawal → vasomotor instability → sympathetic surges → sinus tachycardia, ectopics. The relationship between flushing and palpitations is direct: the same autonomic discharge causes both |
| Drugs (e.g. caffeine, cocaine) [3] | Patients may not volunteer recreational drug use; clinicians may forget to ask about caffeine/energy drink intake | Caffeine: adenosine-receptor antagonism → ↑sympathetic + ↑catecholamines. Cocaine: blocks noradrenaline reuptake + direct Na⁺ channel blockade → sinus tachycardia, ectopics, VT, coronary vasospasm |
| Mitral valve disease [3] | Murmur may be subtle; MVP click easily missed if not auscultated in the correct position | MS: left atrial pressure overload → atrial dilatation → AF (classic association). MVP: myxomatous degeneration → stretch-activated ectopics, associated with autonomic dysfunction and SVT. MR: volume overload → hyperdynamic LV + atrial dilatation → AF/ectopics |
| Aortic incompetence [3] | May present primarily with palpitations rather than classic HF symptoms in young patients | Wide pulse pressure → large stroke volume → each beat is forceful (water-hammer pulse) → perceived as pounding. Why? In AR, blood regurgitates back into the LV during diastole → LV volume overload → compensatory ↑SV on next beat |
| Hypoxia/hypercapnia [3] | Considered a respiratory problem, palpitations not connected to the underlying cause | Hypoxia → chemoreceptor activation → ↑sympathetic → sinus tachycardia. Hypercapnia → cerebral vasodilation + systemic sympathetic activation → ↑HR. Also, chronic lung disease is the leading cause of MAT (~60%) [5] |
| Diagnosis | Key Features | Mechanism |
|---|---|---|
| Tick bites (T1–5) [3] | Travel history to endemic areas; paralytic tick toxin | Tick neurotoxin blocks autonomic ganglia → paradoxical tachycardia and arrhythmias |
| Phaeochromocytoma [3] | Classic triad: paroxysmal headache + sweating + palpitation ( > 90% predictive) [9]; 5 P's: Pressure (HT), Pain (headache, chest pain), Palpitation, Perspiration, Pallor (vasoconstriction) [10]; paroxysmal HTN; young-onset resistant HTN | Episodic catecholamine surges from chromaffin cell tumour → ↑HR, ↑contractility, ↑BP. Palpitations (70%) [9]. Why pallor and not flushing? Because noradrenaline causes α₁-mediated vasoconstriction → pallor (phaeochromocytoma patients sweat but do not flush [9]) |
Masquerades checklist: Depression, Diabetes (indirect), Drugs (see list), Anaemia, Thyroid disorder (hyperthyroidism), Spinal dysfunction [3]
These are conditions that "masquerade" as other diseases. In the context of palpitations:
| Masquerade | How It Masquerades | Mechanism |
|---|---|---|
| Depression [3] | Patients present with somatic complaints (palpitations) rather than mood symptoms; SSRIs/SNRIs used to treat depression can themselves cause palpitations | Depression → chronic ↑cortisol and sympathetic tone → sinus tachycardia; SSRIs → serotonergic effects on cardiac 5-HT₄ receptors → atrial ectopics |
| Diabetes (indirect) [3] | Palpitations from hypoglycaemia episodes (insulin/sulfonylurea therapy) rather than DM itself; also DM → autonomic neuropathy → resting tachycardia | Hypoglycaemia → counter-regulatory adrenaline surge → palpitation, sweating, anxiety, tremor, tachycardia [15]; autonomic neuropathy → loss of vagal tone → fixed tachycardia |
| Drugs [3] | As detailed above — any prescribed, OTC, or recreational substance | Drug-specific (see above) |
| Anaemia [3] | Palpitations may be the presenting symptom of occult GI bleed or menorrhagia | ↓Hb → ↓O₂ carrying capacity → compensatory ↑HR + ↑SV → regular, relatively fast pounding (90–120 bpm) [1][2]. The heart beats harder and faster to maintain O₂ delivery |
| Thyroid disorder, hyperthyroidism [3] | Consider hyperthyroidism as a cause of atrial fibrillation or sinus tachycardia even if the clinical manifestations are not apparent [3]; elderly thyrotoxicosis may present with AF alone ("apathetic thyrotoxicosis") | T3/T4 ↑β₁-receptor expression on cardiomyocytes → ↑chronotropy and inotropy; ↑Na⁺/K⁺-ATPase → shortened atrial refractory period → facilitates AF; ↓SVR → ↑CO → hyperdynamic state |
| Spinal dysfunction [3] | Upper thoracic (T1–5) dysfunction can refer pain/discomfort to the chest, perceived as palpitations or chest tightness | Spinal nerve root irritation at T1–T5 → somatic referred sensation to anterior chest wall → misinterpreted as cardiac by the patient |
Is the patient trying to tell me something? Quite likely. Consider cardiac neurosis, anxiety. [3]
| Diagnosis | Key Features | Mechanism |
|---|---|---|
| Panic disorder [6] | Recurrent, unexpected panic attacks with palpitations, sweating, trembling, SOB, chest pain, paraesthesia, fear of dying [6]; median age of onset 24y, M:F ≈ 1:2 [6]; also known as: irritable heart, Da Costa's syndrome [6] | Cognitive downward spiral: anxiety → somatic symptoms → catastrophic interpretation ("I'm having a heart attack") → more anxiety → more symptoms. The palpitations are real (genuine sinus tachycardia from sympathetic activation) but the perceived threat is disproportionate [6] |
| GAD | Chronic generalised worry with autonomic arousal: sweating, palpitations, dry mouth, epigastric discomfort, dizziness [16] | Chronic low-grade sympathetic hyperactivation → persistent mild sinus tachycardia + heightened interoception |
| Somatoform disorder | CVS/resp symptoms including chest pain, SOB, palpitations are common [7]; excessive health-seeking, doctor-shopping, repeated negative workups | Amplified somatic awareness without organic disease; possibly altered central processing of interoceptive signals |
The Anxiety vs Arrhythmia Trap
Never assume palpitations are "just anxiety" without at least a basic ECG. Young women are particularly at risk of being dismissed — yet AVNRT (the most common paroxysmal SVT) has a female predominance and presents in the same demographic as panic disorder. The key differentiator: AVNRT has sudden onset and offset and responds to vagal manoeuvres [1][2], while anxiety-related palpitations build gradually with escalating worry. Always ask: "Does it start and stop like a switch, or does it build up gradually?"
Differentiating Key DDx Pairs
Some DDx pairs are notoriously confusing. Here's how to tell them apart:
Both are irregularly irregular. The distinction:
- AF: no discernible P waves, chaotic baseline fibrillatory waves [1]
- MAT: ≥3 P wave morphologies in the same lead, flat isoelectric line preserved [5] — you can see discrete P waves, they just look different from each other
- Clinical context: MAT is a/w pulmonary disease (~60%) [5]; AF is a/w age, HTN, valvular disease
Both present as regular narrow-complex tachycardia with sudden onset/offset:
- AVNRT: no accessory pathway, circuit is within the AV node; P waves buried in or immediately after QRS ("pseudo-R' in V1, pseudo-S in inferior leads"); the most common paroxysmal SVT; young, F > M [1][2]
- AVRT: requires an accessory pathway; in sinus rhythm, delta wave may be visible (WPW pattern); during orthodromic AVRT, retrograde P waves visible after QRS with longer RP interval than AVNRT
This is the most critical DDx in acute tachycardia management:
- Assume VT until proven otherwise — this is safer
- VT features: AV dissociation (P waves marching through independently), capture/fusion beats, concordance across precordial leads, very broad QRS ( > 160ms), northwest axis
- SVT with aberrancy: preceding P waves, typical RBBB/LBBB morphology, prior documented BBB
| Feature | Anxiety/Panic | Cardiac Arrhythmia |
|---|---|---|
| Onset | Builds gradually with escalating worry | Sudden, like a light switch [1][2] |
| Offset | Gradual resolution | Sudden or terminated by vagal manoeuvres |
| Rate perception | "Racing" but usually 90–120 bpm | Often > 150 bpm |
| Associated Sx | Hyperventilation, paraesthesia, depersonalisation, fear of dying [6] | Syncope, chest pain, polyuria (SVT) |
| Trigger | Stress, no objective danger [6] | Exercise, rest (depends on type), alcohol |
| ECG during attack | Sinus tachycardia | Specific arrhythmia pattern |
| Physical findings between attacks | Normal | May have murmur, delta wave, prolonged QT |
Clinical Pearl
Panic disorder was historically known as "irritable heart" and "Da Costa's syndrome" [6] — the cardiac-sounding names reflect how easily it mimics cardiac disease. Always perform at least one ECG and consider Holter monitoring before labelling palpitations as "functional." Conversely, don't forget that panic disorder is common (lifetime risk 4.7%) and a genuine diagnosis that deserves treatment, not dismissal.
For completeness and exam revision, here is the arrhythmia-specific DDx organised by site:
| Site | Tachyarrhythmias | Bradyarrhythmias |
|---|---|---|
| SA node | Sinus tachycardia (ST) | Sinus bradycardia, Sick sinus syndrome, Sinus arrest, Sinoatrial block |
| Atrial muscle | Atrial tachycardia (AT), Atrial flutter (AFL), Atrial fibrillation (AF), Atrial premature beats/ectopics (APB) | Atrial escape |
| AV node | AV re-entrant tachycardia (AVRT), AV nodal re-entrant tachycardia (AVNRT), Junctional tachycardia | AV blocks, Junctional escape |
| Ventricles | Ventricular tachycardia (VT), Ventricular fibrillation (VF), Ventricular premature beats/ectopics (VPB) | Ventricular escape |
| Condition | HK Relevance | Key Distinguishing Feature |
|---|---|---|
| AF | Ageing population; most common sustained arrhythmia in HK | Irregularly irregular; risk stratification for stroke (CHA₂DS₂-VASc) is standard practice |
| Thyrotoxic periodic paralysis | Up to 2% of Asian thyrotoxic patients; young Asian male [8] | Palpitations + paralysis + hypoK; always check TFT in any young Asian male with hypoK |
| Apical HCMP | 25–30% of HCMP in Japan and HK [12] | Palpitations + diastolic HF + giant T-wave inversions on ECG; often misdiagnosed as IHD |
| Rheumatic heart disease | Still seen in older HK patients and new immigrants from mainland China | MS → AF; MR → volume overload + ectopics |
| NPC-related radiation effects | Post-radiotherapy for NPC can cause thyroid dysfunction (hypo or hyper) and carotid disease | Ask about prior NPC treatment in any HK patient with new palpitations |
High-Yield DDx Summary for Exams (Murtagh Framework) [3]:
Probability diagnosis: Anxiety, Premature beats (ectopics), Sinus tachycardia, SVT, Drugs
Serious disorders not to be missed: MI/angina, AF/AFL, VT, Bradycardia/heart block, SSS, TdP, Long QT, WPW, HypoK/HypoMg, Hypoglycaemia
Pitfalls: Fever/infection, Pregnancy, Menopause, Caffeine/cocaine, Mitral valve disease, AR, Hypoxia/hypercapnia
Rarities: Tick bites, Phaeochromocytoma
Masquerades: Depression, Diabetes, Drugs, Anaemia, Thyrotoxicosis, Spinal dysfunction
Psychiatric: Cardiac neurosis, Anxiety, Panic disorder
High Yield Summary
-
Four DDx categories: (a) Tachyarrhythmias, (b) Hyperdynamic circulation, (c) Bradyarrhythmias, (d) Non-cardiac/functional.
-
Most common causes: Anxiety, ectopics (APB/VPB), sinus tachycardia, SVT, drugs — these account for the vast majority of presentations.
-
Must not miss: MI, AF/AFL, VT, heart block, SSS, TdP, LQTS, WPW, hypoK/hypoMg, hypoglycaemia.
-
Bedside sorting: Get the patient to tap out the rhythm. Irregular = AF/MAT. Skip + pause = ectopics. Sudden rapid regular = re-entrant SVT. Gradual fast = sinus tachycardia. Slow heavy = bradycardia. Moderate regular + systemic symptoms = hyperdynamic state.
-
Key DDx pair — anxiety vs AVNRT: Both common in young women. Sudden onset/offset + vagal termination = AVNRT. Gradual build-up with worry cascade = anxiety/panic. Never label palpitations as anxiety without at least one ECG.
-
Thyrotoxicosis is the great imitator: Check TFTs even if clinical manifestations not apparent — can cause AF, sinus tachycardia, or TPP (in Asian males).
-
WPW danger: Pre-excited AF can conduct rapidly → VF → SCD. Contraindication: AV nodal blockers (digoxin, verapamil, diltiazem) in known WPW with AF.
-
HK-specific: AF (ageing), TPP (young Asian males), apical HCMP (25–30% of HK HCMP), RHD in older/immigrant patients.
Active Recall - Palpitations Differential Diagnosis
References
[1] Senior notes: Ryan Ho Cardiology.pdf (p61, Section 2.3 Palpitations) [2] Senior notes: Ryan Ho Fundamentals.pdf (p206, Section 3.1.3 Palpitations) [3] Lecture slides: murtagh merge.pdf (p72–74, Palpitations) [5] Senior notes: Ryan Ho Cardiology.pdf (p92, Focal and Multifocal Atrial Tachycardia) [6] Senior notes: Ryan Ho Psychiatry.pdf (p178–179, Panic Disorder) [7] Senior notes: Ryan Ho Psychiatry.pdf (p202, Somatic Symptom Disorder) [8] Senior notes: Ryan Ho Endocrine.pdf (p29, Thyrotoxic Periodic Paralysis) [9] Senior notes: Ryan Ho Endocrine.pdf (p66, Phaeochromocytoma) [10] Senior notes: maxim.md (Section on Phaeochromocytoma, 5 P's) [12] Senior notes: Ryan Ho Cardiology.pdf (p169, Apical HCMP) [13] Senior notes: Ryan Ho Critical Care.pdf (p28, Cardiac Arrest) [14] Senior notes: Ryan Ho Cardiology.pdf (p83, Sick Sinus Syndrome) [15] Senior notes: Ryan Ho Endocrine.pdf (p94, Hypoglycaemia) [16] Senior notes: Ryan Ho Psychiatry.pdf (p173, GAD)
Diagnostic Criteria
Palpitations themselves have no formal "diagnostic criteria" — they are a symptom, not a disease. The diagnostic process is about identifying the underlying cause. However, several specific diagnoses that present with palpitations do have formal criteria, and you need to know them.
A diagnosis of benign or functional palpitations is essentially one of exclusion. You can be reasonably confident the palpitations are benign when:
- History is consistent with ectopics or anxiety (gradual onset, no syncope, no red flags)
- Resting ECG is normal (no delta wave, no prolonged QT, no ST changes, no structural abnormalities)
- Basic bloods are normal (no anaemia, normal electrolytes, normal TFTs, normal glucose)
- No structural heart disease on examination or echocardiography
- No red flag features: syncope, exertional palpitations, FHx of SCD < 40y, known cardiomyopathy
The Real Question
The diagnostic criteria you need to know are not for "palpitations" per se, but for the specific arrhythmias and conditions that cause them. The diagnostic workup is a systematic process of elimination guided by clinical probability.
Diagnostic Criteria for Key Underlying Conditions
- ECG criteria: Absence of consistent P waves, replaced by fibrillatory waves (irregular baseline undulations); irregularly irregular RR intervals; narrow QRS (unless coexistent BBB or pre-excitation)
- Duration classification: Paroxysmal ( < 7 days, self-terminating), Persistent (>7 days or requiring cardioversion), Long-standing persistent ( > 12 months), Permanent (accepted by patient and clinician)
- A single-lead ECG recording of ≥30 seconds showing AF is sufficient for diagnosis (2024 ESC guidelines)
A. Recurrent unexpected panic attacks, i.e. an abrupt surge of intense fear/discomfort that reaches a peak within minutes and during which time ≥4 of following symptoms occur: [6] (1) Palpitations, pounding heart or ↑HR (2) Sweating (3) Trembling or shaking (4) Sensations of SOB or smothering (5) Feelings of choking (6) Chest pain or discomfort (7) Nausea or abdominal distress (8) Feeling dizzy, unsteady, light-headed, or faint (9) Chills or heat sensations (10) Paraesthesias (11) Derealization or depersonalization (12) Fear of losing control or 'going crazy' (13) Fear of dying [6] B. ≥1 attacks has been followed by ≥1mo of ≥1 of following: (1) persistent concern/worry about additional panic attacks or their consequences (2) a significant maladaptive change in behaviour related to the attacks [6] C. Not attributable to substance or another medical condition [6] D. Not better explained by another mental disorder [6]
Note: Criterion C is critical — you must exclude organic causes (thyrotoxicosis, phaeochromocytoma, arrhythmias, hypoglycaemia) before diagnosing panic disorder. Palpitations are literally criterion A(1).
Relevant because MI/angina [3] is a "serious disorder not to be missed":
Detection of rise and/or fall of cardiac biomarker values (preferably cTn) with ≥1 value above 99th URL; plus ≥1 of: (1) Symptoms of ischaemia (2) New or presumed new significant ST-T changes or new LBBB (3) Development of pathological Q waves (4) Imaging evidence of new loss of viable myocardium or new RWMA (5) Identification of an intracoronary thrombus [17]
| Arrhythmia | ECG Criteria | Why These Features Occur |
|---|---|---|
| Sinus tachycardia | Rate > 100 bpm, normal P before every QRS, normal P-axis (upright in II, inverted in aVR) | SA node fires faster → same P morphology, just more frequent |
| APB | Premature P wave with abnormal morphology ± compensatory pause; narrow QRS | Ectopic atrial focus fires early → P looks different because the depolarisation vector originates from a different site |
| VPB | Premature wide QRS ( > 120ms) without preceding P wave; compensatory pause; discordant T wave | Ectopic ventricular focus → slow cell-to-cell conduction (no Purkinje) → wide QRS; T wave opposite to QRS direction |
| AF | No P waves, irregular fibrillatory baseline, irregularly irregular RR intervals | Multiple chaotic re-entrant wavelets → no organised atrial depolarisation → random ventricular activation through AV node |
| AFL | Sawtooth flutter waves (best seen in II, III, aVF, V1) at ~300/min; regular ventricular rate (usually 2:1 block → ~150 bpm) | Macro-re-entry around tricuspid annulus → rhythmic atrial depolarisation at fixed rate |
| AVNRT | Narrow complex, regular, 150–250 bpm; P waves buried in QRS or just after (pseudo-R' in V1, pseudo-S in inferior leads) | Simultaneous atrial and ventricular activation because circuit is so compact that retrograde P occurs during QRS |
| AVRT (WPW) | During sinus rhythm: short PR ( < 120ms), delta wave (slurred QRS upstroke), wide QRS. During orthodromic AVRT: narrow complex SVT with retrograde P after QRS | Delta wave = pre-excitation via accessory pathway bypassing AV node delay; during AVRT, the circuit uses AV node antegradely (narrow QRS) and accessory pathway retrogradely |
| VT | Wide QRS ( > 120ms), rate > 100 bpm, AV dissociation, capture beats, fusion beats, concordance across precordial leads | Ventricular origin → cell-to-cell conduction without Purkinje → wide QRS; atria and ventricles depolarise independently (AV dissociation) |
| Long QT | QTc > 500ms (significant risk), > 470ms in males or > 480ms in females (Bazett correction: QTc = QT / √RR) | Delayed ventricular repolarisation from K⁺/Na⁺ channelopathy → ↑window for early afterdepolarisations → TdP |
| TdP | Polymorphic VT with sinusoidal oscillation of QRS axis ("twisting of the points") on a background of prolonged QT | EADs trigger polymorphic VT; rotating axis because activation wavefront shifts continuously |
| Brugada | Coved ST elevation ≥2mm in V1–V3 followed by negative T wave (Type 1 = diagnostic) | Na⁺ channel dysfunction → transmural voltage gradient during repolarisation → predisposition to VF |
The approach to a patient presenting with palpitations follows a structured pathway that moves from clinical assessment → risk stratification → targeted investigations.
Step-by-Step Clinical Approach
The Golden Rule of Palpitation Diagnosis
The single most valuable diagnostic event is capturing an ECG during symptoms. A normal ECG during palpitations essentially excludes arrhythmia as the cause. A normal ECG between episodes tells you relatively little — it only excludes resting abnormalities like WPW pattern, prolonged QT, or structural changes.
Investigation Modalities
A. First-Line Investigations — The "Palpitations Checklist"
A checklist includes: FBE, TFTs, serum glucose, urea, electrolytes and magnesium, ECG, cardiac enzymes, echocardiography, Holter monitoring [3]
Let's go through each systematically, explaining why each test is ordered and what you're looking for.
Why it's done: The single most important first-line investigation. It gives you a snapshot of the heart's electrical activity right now.
When to do it: Every patient presenting with palpitations. Ideally during symptoms — this is diagnostic gold.
The ideal time to examine the patient is during the palpitations. If not, the examination is usually normal [3]
Key findings and their interpretation:
| ECG Finding | Diagnosis Suggested | Pathophysiology |
|---|---|---|
| Normal sinus rhythm | Symptoms may be benign; does NOT exclude paroxysmal arrhythmia | Between attacks, conduction system functions normally |
| Sinus tachycardia | Secondary cause (fever, anaemia, thyrotoxicosis, anxiety, drugs) | ↑SA node automaticity from sympathetic drive |
| Delta wave + short PR | WPW syndrome [3] — even if asymptomatic at time of ECG | Accessory pathway conducts faster than AV node → pre-excitation (delta wave = early slow ventricular activation before His-Purkinje catches up) |
| Prolonged QTc | Long QT syndrome [3]; drugs; hypoK, hypoMg [3] | Delayed repolarisation → ↑risk of EADs → TdP |
| Ectopic beats (APB/VPB) | Premature beats [3] — most common cause of palpitations | Ectopic focus fires prematurely |
| AF pattern | Atrial fibrillation [3] | Chaotic atrial activation |
| Flutter waves | Atrial flutter [3] | Organised macro-re-entry in RA |
| Wide complex tachycardia | VT until proven otherwise | Ventricular origin or SVT with aberrancy |
| ST changes | MI/ischaemia [3] | Myocardial injury current |
| LVH criteria | HCMP, hypertensive heart disease → substrate for arrhythmia | ↑LV mass → ↑voltage on ECG |
| Giant T-wave inversions in precordial leads | Apical HCMP (high prevalence in HK) | Apical hypertrophy creates repolarisation abnormality |
| Brugada pattern (coved ST in V1-3) | Brugada syndrome | Na⁺ channel dysfunction → repolarisation abnormality |
| Epsilon waves in V1-V3 | ARVC (arrhythmogenic RV cardiomyopathy) | Fatty/fibrotic replacement of RV myocardium → delayed RV activation |
Technical note on ECG interpretation [18]:
- Speed = 25mm/s (1s = 5 large squares) → Rate = 300 / number of large squares between R-R [18]
- Amplitude = 1mV/cm (2 large squares = 1mV) [18]
- Limb leads look at heart in frontal plane; Chest leads in horizontal plane [18]
- Cardiac rhythm identified from whichever lead showing P wave most clearly (usually lead II) [18]
2. Blood Tests
Why: To detect anaemia [3] — a common and easily treatable masquerade.
| Finding | Interpretation |
|---|---|
| ↓Hb | Anaemia → hyperdynamic circulation → sinus tachycardia / ↑awareness of heartbeat |
| ↑WCC | Infection/fever → sinus tachycardia |
| ↓Platelets or ↑Platelets | Haematological disorder; thrombocytosis → reactive (IDA causes reactive thrombocytosis [19]) |
Why: Consider hyperthyroidism as a cause of atrial fibrillation or sinus tachycardia even if the clinical manifestations are not apparent [3]. This is the single most commonly missed endocrine cause.
| Finding | Interpretation |
|---|---|
| ↓TSH, ↑fT4 | Overt thyrotoxicosis → AF, sinus tachycardia, ectopics, ↑contractility |
| ↓TSH, normal fT4/T3 | Subclinical hyperthyroidism — still a risk factor for AF, especially in elderly |
| ↑TSH, ↓fT4 | Hypothyroidism — can cause bradycardia (less commonly palpitations, but important) |
Diagnostic Ix: by TFT (TSH most sensitive). ↓TSH ↑T3 ↑fT4: diagnostic of thyrotoxicosis (TSH usually undetectable) [20]
Why: Hypoglycaemia (type 1 diabetes) [3] causes adrenergic symptoms including palpitation, sweating, anxiety, tremor, tachycardia [15].
| Finding | Interpretation |
|---|---|
| < 3.9 mmol/L (with symptoms) | Hypoglycaemia → counter-regulatory catecholamine surge → sinus tachycardia |
| Elevated | DM → check for DKA (can cause hypoK → arrhythmia) |
Why: Hypokalaemia and hypomagnesaemia [3] are the electrolyte disturbances that most commonly cause arrhythmias.
| Finding | Interpretation | Arrhythmia Risk |
|---|---|---|
| ↓K⁺ ( < 3.5 mmol/L) | Diuretics, vomiting, diarrhoea, RTA, Conn's syndrome | ↑Resting membrane potential → delayed repolarisation → ↑QT → U waves → ectopics, VT, TdP |
| ↓Mg²⁺ ( < 0.7 mmol/L) | Often coexists with hypoK; diuretics, alcohol, PPI use | Mg²⁺ stabilises K⁺ channels; depletion → refractory hypoK + independent pro-arrhythmic effect |
| ↑K⁺ ( > 5.5 mmol/L) | Renal failure, K-sparing diuretics, DKA, ACEi/ARBs | ECG changes: 6-7 mmol/L (tall peaked T), 8-10 (wide QRS), 11 (sine wave), 10-12 (VF) [21] |
| ↑Urea/Cr | Renal failure → hyper/hypoK, fluid overload → HF → palpitations | Uraemia is itself pro-arrhythmic |
| ↓Ca²⁺ | Hypoparathyroidism, CKD, massive transfusion | Prolonged QT → risk of TdP |
Why: To exclude MI/angina [3] when palpitations are associated with chest pain or haemodynamic compromise.
| Marker | Interpretation |
|---|---|
| ↑hs-cTnI/T (rise and/or fall with at least 1 value > 99th percentile URL) | Myocardial injury — Type 1 MI (ACS) vs Type 2 MI (demand ischaemia from tachyarrhythmia) [17] |
| ↑NT-proBNP/BNP | Heart failure — particularly if palpitations are from tachycardia-induced cardiomyopathy or AF with fast ventricular rate |
Type 2 MI in Tachyarrhythmia
A sustained tachycardia itself can cause troponin elevation (Type 2 MI) through supply-demand mismatch — ↑HR → ↓diastolic time → ↓coronary perfusion + ↑myocardial O₂ demand. This does NOT necessarily mean the patient has ACS. Context is everything.
Why: To assess for structural heart disease — the substrate for many dangerous arrhythmias.
Indications: Not needed for every patient with palpitations. Order when:
- Suspected structural heart disease (abnormal examination, abnormal ECG)
- Syncope or presyncope with palpitations
- Sustained tachyarrhythmia documented
- Murmur on examination
- Young patient with FHx of SCD or cardiomyopathy
| Finding | Diagnosis | Clinical Significance |
|---|---|---|
| Asymmetric septal hypertrophy (ASH) + SAM | HCMP | Substrate for VT/VF and AF; risk of SCD |
| Apical hypertrophy with spade-like LV cavity | Apical HCMP (HK-relevant) | Usually more benign than obstructive HCMP |
| Dilated LV with ↓LVEF | DCMP | Substrate for VT; risk of thromboembolism |
| Mitral stenosis with ↑LA size | Rheumatic MS → AF | LA dilatation provides substrate for AF |
| Mitral valve prolapse with MR | MVP | Associated with ectopics, SVT, rarely VT |
| Aortic regurgitation | AR → hyperdynamic palpitations | Wide pulse pressure → forceful beats |
| RV dilatation with fatty infiltration | ARVC | Substrate for RV-origin VT |
| Regional wall motion abnormalities | Prior MI → scar-related VT | Re-entrant VT around scar |
Why: Most palpitations are paroxysmal — the resting ECG will be normal. You need to catch the arrhythmia in the act.
Principle: Continuous ECG recording over 24–48 hours (or up to 7 days with extended Holter) while the patient goes about daily life. Patient keeps a diary noting when symptoms occur → allows correlation of symptoms with rhythm.
Key point: The diagnostic yield depends on symptom frequency:
- Daily symptoms → 24h Holter is appropriate (yield ~50%)
- Weekly symptoms → Extended Holter (7-day) or event recorder (yield improves to 65-85%)
- Monthly or less frequent → External loop recorder (2-4 weeks) or implantable loop recorder (ILR)
| Holter Finding | Interpretation |
|---|---|
| Symptoms + arrhythmia at same time | Diagnostic correlation — the arrhythmia is the cause |
| Symptoms + normal rhythm at same time | Arrhythmia excluded as cause → think non-arrhythmic DDx (anxiety, hyperdynamic, etc.) |
| Arrhythmia present but no symptoms | Arrhythmia exists but is not the cause of patient's symptoms (incidental) |
| No symptoms + no arrhythmia | Non-diagnostic — extend monitoring duration |
| Frequent ectopics ( > 10% burden on 24h Holter) | May indicate risk of tachycardia-induced cardiomyopathy; consider treatment |
Event recorder (external):
- Patient-activated device worn for 2-4 weeks
- When symptoms occur, patient presses a button → device saves the preceding 30-60 seconds and the following 30-60 seconds of ECG
- Advantage: Much longer monitoring window than Holter
- Limitation: patient must be conscious and able to activate
Implantable loop recorder (ILR) (e.g., LINQ device):
- Small device implanted subcutaneously in the left parasternal area under local anaesthesia
- Continuous monitoring for up to 3 years
- Auto-detects arrhythmias + patient can activate during symptoms
- Indication: Infrequent but clinically significant episodes (especially syncope with suspected arrhythmia), after non-diagnostic Holter/event recorder
- Yield: Up to 90% diagnostic yield for recurrent unexplained syncope
B. Second-Line / Targeted Investigations
These are not done routinely for all patients but are directed by clinical suspicion.
Why: For palpitations that are exercise-induced — During exercise: think PSVT, AF and VT [1][2]
Principle: Graded exercise on treadmill or bicycle with continuous ECG monitoring. Provokes arrhythmias that are catecholamine-dependent.
| Finding | Interpretation |
|---|---|
| SVT induced by exercise | Catecholamine-sensitive SVT |
| VT induced by exercise | Structural heart disease (post-MI scar VT) or catecholaminergic polymorphic VT (CPVT) — very important in young patients with exertional syncope |
| ST depression with exercise | Ischaemia → demand ischaemia as cause of palpitations |
| Inappropriate sinus tachycardia | Consider IST (inappropriate sinus tachycardia syndrome) |
Why: The definitive invasive test to characterise arrhythmia mechanism. Catheters are placed inside the heart to map the electrical activation and provoke arrhythmias in a controlled setting.
Indications:
- Pre-ablation mapping (AVNRT, AVRT/WPW, AFL, VT)
- Risk stratification (e.g., inducible VT in post-MI patients)
- When non-invasive monitoring has failed to capture the arrhythmia but clinical suspicion remains high
What it tells you: Exact mechanism (re-entry vs automaticity vs triggered), location of the circuit/focus, suitability for catheter ablation
Why: The gold standard for myocardial tissue characterisation — particularly useful for:
| Indication | What CMR Shows |
|---|---|
| HCMP evaluation | Distribution and degree of hypertrophy, late gadolinium enhancement (LGE) = fibrosis/scar = substrate for VT |
| ARVC evaluation | Fatty infiltration of RV, RV dilatation, wall motion abnormalities (modified Task Force criteria for ARVC) |
| Myocarditis | Oedema (acute inflammation) + LGE in mid-wall/epicardial pattern (cf. subendocardial in ischaemia) |
| DCMP evaluation | Degree of dilatation, LGE pattern, aetiological clues |
| Sarcoidosis | LGE in basal septum — cardiac sarcoid is a cause of VT and heart block |
Why: When ischaemia is suspected as the driver of palpitations (exercise-induced symptoms, risk factors for CAD).
Indication: screening and diagnosis of coronary artery disease. Determine adequacy of blood flow ± stress (functional in nature → detect a haemodynamically significant anatomical endpoint, i.e., flow-limiting coronary stenosis defined by ≥50% diameter stenosis) [22]
- At rest, partial coronary stenosis limits blood flow but collaterals + vasodilation maintain perfusion [22]
- With stress, vessels supplying normal myocardium also dilate → blood siphoned away from affected territory ('coronary steal') → cold spots [22]
- Ischaemia → cold spots with stress only; Infarct → cold spots at rest AND stress [22]
10. Specific Endocrine Investigations
Biopsy is NOT required: high risk of hypertensive crisis and haematoma [10]
| Test | Details | Interpretation |
|---|---|---|
| 24h urine catecholamines + fractionated metanephrines [10] | Most sensitive (continuous release). Abnormal if > 2× elevation. False positives: stress, OSA, drugs (TCA, α-agonist, levodopa → stop 1 week) [10] | Sens 98% Spec 98% [9] |
| Plasma fractionated metanephrines [10] | Most specific but needs indwelling catheter > 30min. Preferred in chronic renal failure [10] | Sens 96-100% Spec 85-89% [9] |
| CT with low-osmolar contrast / T2-MRI [10] | Anatomical localisation. CT: alpha blockade prior to IV contrast due to risk of HT crisis. Low-osmolar contrast safe even without alpha/beta blockade [10] | Localise adrenal or extra-adrenal tumour |
| I-123 MIBG scan [10] | MIBG = metaiodobenzylguanidine, NE analog taken up by phaeochromocytoma [10] | Functional localisation, especially for extra-adrenal or metastatic disease |
| 68Ga-DOTATATE PET-CT [10] | Detect metastatic disease | Superior sensitivity for metastatic phaeochromocytoma/paraganglioma |
| Test | Finding | Interpretation |
|---|---|---|
| TSH (most sensitive) [20] | ↓TSH (usually undetectable in overt thyrotoxicosis) | Screening test of choice |
| fT4, T3 | ↑fT4 ± ↑T3 | Confirms thyrotoxicosis |
| TRAb (anti-TSHr) | Positive | Specific for Graves' disease; prognostic for relapse [20] |
| Thyroid scintigraphy | Diffuse ↑uptake = Graves'; heterogeneous ↑uptake = toxic MNG; focal ↑uptake = toxic adenoma; diffuse ↓uptake = destructive thyroiditis vs factitious [20] | Aetiological differentiation when clinically uncertain |
Diagnosis confirmed by Whipple's triad: (1) Symptoms compatible with hypoglycaemia, (2) Low blood glucose coinciding with time of symptoms, (3) Resolution of symptoms with correction of hypoglycaemia [15]
| Symptom Frequency | Best Monitoring Strategy | Rationale |
|---|---|---|
| Symptoms occurring NOW | 12-lead ECG immediately | Capture the arrhythmia in real-time — diagnostic gold |
| Daily or near-daily | 24-48h Holter | High probability of capturing an event within recording window |
| Weekly | 7-day extended Holter or external event recorder | Need longer monitoring to catch infrequent events |
| Monthly | External loop recorder (2-4 weeks) | Even longer window; patient-activated |
| Very infrequent / unexplained syncope | Implantable loop recorder (ILR) | Up to 3 years of continuous monitoring |
| Exercise-triggered | Exercise stress test | Reproduce the arrhythmia under controlled conditions |
| Suspected structural heart disease | Echocardiography ± Cardiac MRI | Assess substrate (hypertrophy, scar, dilatation, valvular disease) |
| High suspicion, non-diagnostic non-invasive | Electrophysiology study (EPS) | Definitive invasive characterisation and potential ablation |
| Suspected Diagnosis | Key Investigations | Diagnostic Finding |
|---|---|---|
| Ectopics | ECG, Holter | APB (premature narrow QRS + abnormal P) or VPB (premature wide QRS, no P) |
| AF | ECG, Holter | Absent P, fibrillatory baseline, irregularly irregular RR |
| SVT (AVNRT/AVRT) | ECG during attack, EPS | Narrow complex regular tachycardia; EPS defines mechanism |
| WPW | Resting ECG | Delta wave + short PR + wide QRS |
| VT | ECG, Holter, EPS | Wide complex tachycardia + AV dissociation |
| Long QT | ECG | QTc > 470ms (M) or > 480ms (F); ± genetic testing |
| Anaemia | FBE [3] | ↓Hb, ↓MCV (if IDA), ↓reticulocytes |
| Thyrotoxicosis | TFTs [3] | ↓TSH, ↑fT4 |
| Electrolyte disturbance | U&E + Mg [3] | ↓K⁺, ↓Mg²⁺ |
| MI/ACS | ECG + cardiac enzymes [3] | ST changes + ↑hs-cTnI |
| Phaeochromocytoma | 24h urine metanephrines, CT/MRI | > 2× elevation of metanephrines; adrenal mass |
| Structural HD (HCMP, DCMP) | Echo [3], cardiac MRI | ASH, SAM, ↓LVEF, LGE |
| Panic disorder | Clinical (DSM-5 criteria) after excluding organic causes | ≥4 symptoms during unexpected panic attacks + ≥1mo worry/behavioural change [6] |
Diagnostic tips [3]: A relatively non-specific symptom. [3] Consider hyperthyroidism as a cause of atrial fibrillation or sinus tachycardia even if the clinical manifestations are not apparent. [3] Arrhythmia of sudden onset suggests paroxysmal supraventricular tachycardia (PSVT), atrial flutter/fibrillation or ventricular tachycardia. [3] Common triggers for premature beats and PSVT are smoking, anxiety and excessive caffeine. [3]
High Yield Summary
-
No formal diagnostic criteria for "palpitations" — the diagnosis is about identifying the underlying cause.
-
12-lead ECG is the single most important first-line investigation. A normal ECG during symptoms essentially excludes arrhythmia. A normal ECG between episodes only excludes resting abnormalities (WPW pattern, prolonged QT, structural changes).
-
Murtagh's investigation checklist: FBE, TFTs, serum glucose, U&E + Mg, ECG, cardiac enzymes, echocardiography, Holter monitoring.
-
Ambulatory monitoring choice depends on symptom frequency: Daily → Holter; Weekly → extended Holter/event recorder; Monthly → external loop recorder; Very infrequent → ILR.
-
The diagnostic correlation: Symptoms + arrhythmia simultaneously = diagnostic. Symptoms + normal rhythm = arrhythmia excluded. Arrhythmia + no symptoms = incidental finding.
-
Always check TFTs — even in patients without obvious thyrotoxic features. Thyrotoxicosis is the great imitator and a common cause of AF.
-
ECG red flags on resting ECG: Delta wave (WPW), prolonged QTc (LQTS/drugs/electrolytes), Brugada pattern, LVH (HCMP), epsilon waves (ARVC), Q waves (prior MI scar → VT substrate).
-
Phaeochromocytoma: Biopsy is NEVER done. Diagnosis by 24h urine fractionated metanephrines (Sens 98%). Localise by CT/MRI + MIBG scan.
-
Panic disorder diagnosis (DSM-5): Requires recurrent unexpected panic attacks with ≥4/13 symptoms + ≥1 month of worry/behavioural change + exclusion of organic causes + not better explained by another mental disorder.
Active Recall - Palpitations Diagnosis and Investigations
[1] Senior notes: Ryan Ho Cardiology.pdf (p61, Section 2.3 Palpitations) [2] Senior notes: Ryan Ho Fundamentals.pdf (p206, Section 3.1.3 Palpitations) [3] Lecture slides: murtagh merge.pdf (p72–74, Palpitations) [6] Senior notes: Ryan Ho Psychiatry.pdf (p178–179, Panic Disorder) [9] Senior notes: Ryan Ho Endocrine.pdf (p66, Phaeochromocytoma) [10] Senior notes: maxim.md (Section on Phaeochromocytoma investigations) [15] Senior notes: Ryan Ho Endocrine.pdf (p94, Hypoglycaemia) [17] Senior notes: Ryan Ho Cardiology.pdf (p127, Universal Definition of MI) [18] Senior notes: Ryan Ho Fundamentals.pdf (p448, ECG Basics) [19] Senior notes: Ryan Ho Haemtology.pdf (p18, Iron Deficiency Anaemia) [20] Senior notes: Ryan Ho Endocrine.pdf (p13, Thyrotoxicosis investigations) [21] Senior notes: Ryan Ho Chemical Path.pdf (p14, Hyperkalaemia ECG changes) [22] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p57, Myocardial Perfusion Imaging)
Management of palpitations is not management of the symptom — it is management of the underlying cause. Think of it this way: palpitations are to arrhythmia what pain is to fracture. You don't treat the pain in isolation; you fix the bone and the pain resolves. Similarly, you identify the cause of the palpitation and treat that.
The management framework has three tiers:
- Immediate stabilisation — Is the patient haemodynamically compromised right now?
- Cause-specific treatment — What is generating the palpitation?
- Long-term prevention — How do we stop it coming back?
Tier 1: Immediate Stabilisation — The Unstable Patient
The first question is always: Is this patient about to die?
Signs of haemodynamic instability in a patient with palpitations:
- Systolic BP < 90 mmHg or ↓ > 40 mmHg from baseline
- Syncope or altered consciousness
- Acute pulmonary oedema (crackles, pink frothy sputum)
- Myocardial ischaemia (chest pain + ST changes)
- Signs of shock (cold peripheries, delayed CRT, oliguria)
If ANY of these are present → don't waste time characterising the arrhythmia in detail. Treat it.
Cardioversion: delivery of a current over a very short interval → depolarize heart → abolish all prevailing abnormal rhythm → hope that SAN will take the lead again as pacemaker [23]
Synchronized shock with QRS complex → avoid R-on-T phenomenon (torsades then VF) [23]
Why synchronised? If you deliver the shock randomly, it could land on the relative refractory period (the T wave) → this can trigger VF. Synchronisation ensures the shock coincides with the QRS (absolute refractory period), when the ventricle is already depolarised and cannot be "surprised" into VF.
| Rhythm | Energy | Notes |
|---|---|---|
| Narrow regular (SVT, AFL) | 50-100J [23] | Lower energy sufficient because organised rhythm |
| Narrow irregular (AF) | 120-200J [23] | Higher energy needed for chaotic rhythm |
| Wide regular (monomorphic VT) | 100J [23] | |
| Polymorphic VT / VF | 200J unsynchronised (defibrillation) | Cannot synchronise with QRS as there is no identifiable QRS |
Requires consent with sedation (midazolam) + analgesics (morphine) as it is quite painful [23]
Absolute C/I: sinus tachycardia (only absolute C/I) [23]
Why is sinus tachycardia the only absolute contraindication? Because sinus tachycardia is an appropriate response — the SA node is driving the rate because of an underlying problem (fever, dehydration, pain, etc.). Shocking the heart won't fix the cause and the tachycardia will simply recur. You need to treat the underlying stimulus.
IV atropine 0.5mg every 3-5min: 1st line for acute symptomatic bradycardia. Max dose: 3mg [24][25]
Why atropine? "Atropine" comes from Atropa belladonna (deadly nightshade). It is an anticholinergic — it blocks muscarinic (M₂) receptors on the SA node and AV node, removing parasympathetic/vagal brake → heart rate ↑.
When atropine doesn't work [24]:
- Transplanted heart (denervated → no effect) — the heart has no vagal innervation after transplant, so blocking vagal tone has no effect
- Mobitz type II or 3rd-degree heart block with wide QRS — the block is below the AV node (infranodal), in non-nodal tissue that doesn't have muscarinic receptors
Alternative drugs if atropine fails [24][25]:
- Dopamine infusion: 2-20 μg/kg/min [25] — β₁ stimulation ↑HR and contractility; also α₁ vasopressor effect at higher doses
- Adrenaline infusion: 2-10 μg/min [24][25] — β₁ ↑HR and contractility
Temporary cardiac pacing [24][25]:
Mechanism: regular delivery of a small direct current to stimulate contraction of the heart [24]
| Type | Description | When |
|---|---|---|
| Transcutaneous pacing (TCP) | External pads; less reliable but easier, 1st-line in emergency [24] | Immediate bridge while preparing TVP |
| Transvenous pacing (TVP) | Catheter in RV via central vein; more definitive with less tissue damage [24] | After TCP, as definitive temporary measure |
Indications: bradycardia with unstable haemodynamic status; standby in 3rd-degree or Mobitz II 2nd-degree HB with stable haemodynamics [24][25]
Use: usually start at 70 ppm, 30 mA. Electrical capture indicated by spike on ECG. Mechanical capture indicated by palpable pulse. Sometimes possible to get electrical without mechanical capture [25]
Shockable rhythms: VF (totally uncoordinated contraction of ventricles), Pulseless VT (LV rate too fast to pump blood effectively). 80% reversed by defibrillation but 10%↓survival per min delay [13]
Full ACLS protocol: CPR (30:2) → Defibrillation (200J biphasic) → Adrenaline 1mg IV q3-5min → Amiodarone 300mg IV after 3rd shock → Continue cycles with reversible cause search (4H's and 4T's)
Tier 2: Cause-Specific Treatment
Once the patient is stabilised, treatment depends entirely on the specific diagnosis.
A. Benign / Functional Palpitations (Anxiety, Ectopics)
This is the most common scenario — a young, healthy patient with ectopics or anxiety-driven palpitations.
This is genuinely therapeutic. Many patients are terrified they have a heart problem. A clear explanation that their heart is structurally normal and the ectopics are benign can be transformative.
Lifestyle modifications — Common triggers for premature beats and PSVT are smoking, anxiety and excessive caffeine [3]:
| Drug | Dose | Mechanism | When to Use |
|---|---|---|---|
| β-blockers (e.g., bisoprolol 1.25-5mg OD, metoprolol 25-50mg BD) | Low dose | Block β₁-adrenoreceptors → ↓HR, ↓automaticity, ↓catecholamine sensitivity of ectopic foci | Frequent, symptomatic ectopics despite lifestyle changes; especially effective for catecholamine-sensitive ectopics |
| Non-dihydropyridine CCBs (e.g., verapamil, diltiazem) | Standard dose | Block L-type Ca²⁺ channels in SA/AV node → ↓HR, ↓automaticity | Alternative if β-blockers contraindicated |
Catheter ablation: Consider for high-burden VPBs ( > 10-15% on Holter) as these can cause tachycardia-mediated cardiomyopathy — the persistent ectopics cause LV dilatation and ↓EF over time.
B. Supraventricular Tachycardia (AVNRT / AVRT)
This is the classic discrete bouts, very rapid ( > 120 bpm), sudden onset, terminated by vagal manoeuvres [1][2] scenario.
Step 1: Vagal manoeuvres [23]
Vagal manoeuvres: carotid sinus massage, Valsalva's manoeuvre, cold packs, cold water [23]
Why do these work? They stimulate the vagus nerve → ↑acetylcholine at the AV node → slows AV nodal conduction → breaks the re-entrant circuit that depends on the AV node.
The modified Valsalva manoeuvre (REVERT trial) has the highest success rate (~43% vs 17% for standard Valsalva): Patient blows against a 10mL syringe for 15 seconds while sitting at 45° → immediately laid flat with legs elevated to 45° for 15 seconds. The leg elevation increases venous return → ↑baroreceptor stretch → ↑vagal tone.
Step 2: IV Adenosine (if vagal manoeuvres fail) [23]
IV adenosine: 6mg IV push followed by NS flush (1st dose), 12mg IV bolus (2nd and 3rd dose if required) [23]
Mechanism: Adenosine ("adeno" = gland, "sine" = without) — activates A₁ receptors on AV nodal cells → opens K⁺ channels → hyperpolarises the cell → transiently blocks AV conduction for ~5-10 seconds → breaks re-entrant circuit.
Why rapid IV push? Adenosine has a half-life of < 10 seconds — it is rapidly metabolised by adenosine deaminase in red blood cells. If you inject slowly, it gets destroyed before reaching the heart.
| Important Points about Adenosine | |
|---|---|
| Diagnostic and therapeutic | If it terminates the tachycardia = confirms AVNRT/AVRT. If it slows the rate transiently revealing flutter waves or AT = it's not AVNRT/AVRT |
| Warn the patient | They will feel a brief but intense chest tightness, flushing, and a sense of impending doom (transient AV block). Lasts < 15 seconds |
| Contraindications | Asthma (adenosine causes bronchospasm via A₂B receptors), 2nd/3rd-degree heart block, known hypersensitivity |
| Caution in WPW with AF | Should NOT be given if unstable or irregular/polymorphic wide-complex tachycardia (may degenerate into VF) [23] |
| Drug interactions | Dipyridamole inhibits adenosine breakdown → ↑effect → use lower dose. Theophylline/caffeine antagonise adenosine → may need higher dose |
Step 3: IV β-blockers or CCBs if adenosine fails
- IV verapamil 5-10mg over 2 min, or IV diltiazem
- IV metoprolol or esmolol
Verapamil 5-15mg IV slowly (C/I if BP low or on BB, beware of post-conversion angina) [26]
Step 4: Synchronised cardioversion if all else fails or patient becomes unstable [23]
| Strategy | Details | Mechanism |
|---|---|---|
| Self-vagal manoeuvres | Teach patient modified Valsalva for self-termination | Empowers patient to abort episodes without hospital |
| β-blockers / CCBs | Daily prophylaxis (e.g., verapamil, diltiazem, metoprolol) | Slows AV nodal conduction → makes it harder for re-entry to sustain |
| "Pill-in-pocket" | Single dose of flecainide or diltiazem taken only when attack starts | Convenient for infrequent attacks; avoids daily medication |
| Catheter ablation | Definitive treatment; success rate > 95% for AVNRT, > 90% for AVRT | Radiofrequency or cryoablation destroys the slow pathway (AVNRT) or accessory pathway (AVRT) |
Catheter ablation is now considered first-line for recurrent SVT in many guidelines (2019 ACC/AHA/HRS) because it is curative. Why wait for lifelong medication when you can fix the circuit permanently?
WPW with Pre-excited AF — A Special Danger
AV nodal blockers (digoxin, verapamil, diltiazem, adenosine) are CONTRAINDICATED in pre-excited AF because they block the AV node but leave the accessory pathway conducting unchecked → all atrial fibrillation impulses conduct rapidly via the accessory pathway → ventricular rate can exceed 300 bpm → VF → death.
Correct treatment: IV procainamide (slows conduction in the accessory pathway) or immediate cardioversion if unstable. Definitive: catheter ablation of accessory pathway.
C. Atrial Fibrillation (AF)
The most common sustained arrhythmia and the one with the most complex management algorithm. Three parallel management streams:
Goal: Slow the ventricular rate to < 110 bpm at rest (lenient target, 2024 ESC guidelines) or < 80 bpm (strict target if still symptomatic).
Why? In AF, the atria fire at 350-600/min. Without the AV node acting as gatekeeper, the ventricles would try to follow → haemodynamic collapse. Rate control drugs slow AV nodal conduction → fewer atrial impulses reach the ventricles.
| Drug Class | Examples | Mechanism | When to Use | Contraindications |
|---|---|---|---|---|
| β-blockers | Bisoprolol, metoprolol, atenolol | Block β₁ → ↓AV conduction, ↓HR | First-line in most patients; particularly if coexistent IHD/HF with preserved EF | Decompensated HF (HFrEF), severe asthma, hypotension |
| Non-DHP CCBs | Verapamil, diltiazem | Block L-type Ca²⁺ channels in AV node → ↓conduction velocity | First-line alternative; good for patients without HF | HFrEF (negative inotrope → ↓↓EF), concurrent β-blocker (risk of asystole) |
| Digoxin | Digoxin 0.0625-0.25mg OD | Inhibits Na⁺/K⁺-ATPase → ↑intracellular Ca²⁺ + ↑vagal tone → slows AV conduction | Second-line; particularly useful in HFrEF (mild positive inotrope); effective at rest but less so during exercise | Hypokalaemia (↑toxicity), hypoMg, renal impairment (dose adjustment), WPW |
| Amiodarone | IV or PO | Class III antiarrhythmic (multiple actions) → slows AV conduction | Acute rate control when above agents fail; haemodynamically compromised patients | Long-term toxicity (thyroid, lung, liver, cornea, skin) |
AF loading with digoxin: 0.25mg IV/PO stat, then 0.25mg PO q8H for 2 more doses, maintenance 0.0625-0.25mg daily [26]
Goal: Restore and maintain sinus rhythm.
When? Preferred when: symptomatic despite rate control, young patient, first episode, HF, no significant LA dilatation.
| Strategy | Details |
|---|---|
| Pharmacological cardioversion | Flecainide (if no structural HD), amiodarone (if structural HD), vernakalant (IV, for recent-onset AF) |
| Electrical cardioversion (DCCV) | Synchronised shock 120-200J [23]; requires ≥3 weeks therapeutic anticoagulation OR TOE-guided approach to exclude LA thrombus |
| Catheter ablation (PVI) | Pulmonary vein isolation — electrically disconnects the pulmonary veins (the main triggers) from the LA. First-line rhythm control in selected patients (2024 ESC). Success rate ~70-80% single procedure, ~85-90% after repeat |
| Antiarrhythmic maintenance | Flecainide/propafenone (no structural HD), amiodarone/sotalol/dronedarone (with structural HD); all have proarrhythmic risk |
Amiodarone for AF: 5 mg/kg IV infusion over 60 mins as loading, maintenance 600-900 mg infusion/24h [26]
AF causes blood stasis in the left atrial appendage → thrombus → systemic embolism → stroke. This is the major morbidity.
CHA₂DS₂-VASc score (decides who needs anticoagulation):
| Letter | Risk Factor | Points |
|---|---|---|
| C | Congestive heart failure | 1 |
| H | Hypertension | 1 |
| A₂ | Age ≥75 | 2 |
| D | Diabetes | 1 |
| S₂ | Stroke/TIA/VTE history | 2 |
| V | Vascular disease (MI, PAD, aortic plaque) | 1 |
| A | Age 65-74 | 1 |
| Sc | Sex category (female) | 1 |
| Score | Recommendation (2024 ESC) |
|---|---|
| 0 (male) or 1 (female) | No anticoagulation |
| 1 (male) | Consider anticoagulation |
| ≥2 (male) or ≥3 (female) | Anticoagulation recommended |
Drug choice: DOACs (dabigatran, rivaroxaban, apixaban, edoxaban) preferred over warfarin in non-valvular AF. Warfarin still used in mechanical valves and moderate-severe MS.
HAS-BLED score: Assesses bleeding risk. High score doesn't mean "don't anticoagulate" — it means "optimise modifiable risk factors."
Atrial flutter: rapid regular atrial activity at 180-350 bpm, mechanism: re-entry via anatomically fixed pathway [5]
| Treatment | Details |
|---|---|
| Acute | Rate control (BB, CCB, digoxin) or cardioversion; IV ibutilide for pharmacological cardioversion |
| Definitive | Catheter ablation of cavotricuspid isthmus — success rate > 95%, very low recurrence. This is considered first-line because flutter tends to be resistant to drug therapy and ablation is so effective |
| Anticoagulation | Same stroke risk as AF → anticoagulate using same CHA₂DS₂-VASc criteria |
Treatment: Correction of contributing factors (↑SN tone aggravates FAT). Acute: BB, CCB (1st line), class IA, IC, III antiarrhythmics (2nd line) ± DCCV. Long-term: maintenance BB/CCB ± catheter ablation or amiodarone if frequent/symptomatic [5]
Treatment: not symptomatic on its own → Tx should be directed to underlying condition [5]
Key: Treat the underlying cause — usually pulmonary disease (~60%), congestive HF, hypoK, hypoMg [5]. Correct electrolytes. IV magnesium may help suppress ectopic foci. Cardioversion is NOT effective (multiple foci — you can't shock away automaticity).
G. Ventricular Tachycardia (VT)
| Scenario | Treatment |
|---|---|
| Haemodynamically unstable / pulseless | Defibrillation (unsynchronised 200J biphasic) per ACLS |
| Haemodynamically stable, sustained monomorphic VT | IV amiodarone: 150mg over 10min, repeat if recur [23]; IV procainamide: 20-50mg/min until arrhythmia suppressed [23]; IV sotalol: 100mg (1.5mg/kg) over 5min [23] |
| Post-MI stable sustained monomorphic VT | Amiodarone 150mg over 10min, repeat 150mg if needed, then 600-1200mg infusion over 24h [26]; Lignocaine 50-100mg IV bolus then 1-4mg/min [26]; Synchronised cardioversion starting with 100J [26] |
| Sustained polymorphic VT | Unsynchronised cardioversion starting with 200J [26] |
| TdP | IV magnesium 2g over 10min (regardless of serum Mg); correct hypoK; stop QT-prolonging drugs; temporary overdrive pacing to ↑HR (shortens QT) |
Why amiodarone? "Amio" from "amiodarone" — developed as an anti-anginal. It turned out to block Na⁺ channels (Class I), β-receptors (Class II), K⁺ channels (Class III), and Ca²⁺ channels (Class IV) — it does everything. This makes it the most effective antiarrhythmic for life-threatening VT, but its multi-channel action also explains its extensive side-effect profile.
| Strategy | Indication |
|---|---|
| ICD (Implantable Cardioverter-Defibrillator) | Secondary prevention: any survived VT/VF arrest. Primary prevention: LVEF ≤35% + NYHA II-III despite optimal medical therapy (SCD-HeFT criteria) |
| Antiarrhythmic drugs | Amiodarone or sotalol as adjunct to ICD to reduce shock frequency |
| Catheter ablation | Recurrent VT despite ICD + drugs; scar-related VT mapping and ablation |
| Treat underlying cause | Revascularisation if ischaemic; correct electrolytes; optimise HF therapy |
| Strategy | Details | Mechanism |
|---|---|---|
| Avoid triggers | QT-prolonging drugs (www.crediblemeds.org), hypoK, hypoMg, intense exercise in LQT1, sudden auditory stimuli in LQT2 | Remove precipitants for EADs |
| β-blockers | Nadolol or propranolol (non-selective) | ↓Sympathetic trigger; ↓HR → but paradoxically also lengthens QT slightly — net effect is protective because EADs are catecholamine-dependent |
| ICD | High-risk patients (previous TdP/arrest, QTc > 500, LQT3) | Backup defibrillation if β-blockers fail |
| Left cardiac sympathetic denervation (LCSD) | Refractory cases | Removes left stellate ganglion → ↓sympathetic input to heart |
| Strategy | Details |
|---|---|
| Asymptomatic WPW pattern | Risk stratification (EPS); if low risk → observe. If high risk (short anterograde refractory period of accessory pathway) → ablation |
| Symptomatic AVRT | Acute: vagal manoeuvres → adenosine → cardioversion. Long-term: catheter ablation (first-line, curative) |
| Pre-excited AF | NEVER give AV nodal blockers (digoxin, verapamil, diltiazem). IV procainamide or immediate cardioversion. Definitive: ablation of accessory pathway |
Permanent AAI/DDD pacing if symptomatic + pause ≥3s, DDD if foresee development of AV nodal disease [14]
| Condition | Pacing Indication |
|---|---|
| Sick sinus syndrome | Permanent pacing (AAI/DDD) if symptomatic + pause ≥3s [14]; no prognostic benefit if asymptomatic [14]; ± anticoagulation if AF [14] |
| Mobitz type II 2nd-degree HB | Permanent pacing (DDD) — high risk of progression to complete HB |
| Complete (3rd-degree) HB | Permanent pacing (DDD) — always indicated regardless of symptoms |
| Mobitz type I (Wenckebach) | Usually benign; pacing only if symptomatic |
Tier 3: Treatment of Non-Arrhythmic Causes
The palpitations resolve when you treat the underlying condition:
| Cause | Treatment | Why It Works |
|---|---|---|
| Anaemia [3] | Treat underlying cause (iron, B12, folate, transfusion if severe) | Restore O₂ carrying capacity → ↓compensatory ↑HR/SV |
| Thyrotoxicosis [3] | β-blockers for symptom control (e.g., propranolol, atenolol) [27]; antithyroid drugs or definitive therapy (RAI/surgery) | Block β₁-adrenoreceptors in heart — relieve palpitations; block β₁ in brain — relieve anxiety; block β₂ in skeletal muscle — relieve tremor [27] |
| Fever/infection [3] | Treat infection; antipyretics | ↓Metabolic demand → ↓sympathetic drive |
| Hypoglycaemia [3] | Oral glucose 15-20g if conscious; IV D50 40mL if unconscious; IM glucagon 1mg if no IV access [15] | Restore euglycaemia → stop counter-regulatory catecholamine surge |
| Electrolyte correction | IV KCl (max 20 mmol/h via central line), IV MgSO₄ | Restore normal resting membrane potential → ↓arrhythmogenicity |
| Drug-related [3] | Stop/reduce offending drug; switch to alternative | Remove the trigger |
| Pregnancy [3] | Reassurance; avoid supine position (IVC compression → reflex tachycardia) | Normal physiological change; resolves post-partum |
Management: Medical therapy: pre-operative prevention of crisis by combined α/β-blockade [28]
Choice: α-blockade by phenoxybenzamine → followed by β-blockade by propranolol [28]
β-blockade alone will cause unopposed α-adrenergic activity → exacerbate HTN. ALWAYS initiate α-blockade before β-blockade → adequate α-blockade indicated by postural BP drop [28]
| Phase | Treatment | Mechanism |
|---|---|---|
| Pre-operative (≥7-14 days) | α-blockade (phenoxybenzamine) → then β-blockade (propranolol); ↑Na diet + fluids | α-blockade reverses vasoconstriction → ↓BP; β-blockade controls reflex tachycardia; fluids reverse catecholamine-induced volume contraction |
| Surgical | Laparoscopic adrenalectomy | Definitive cure |
| Post-operative | Monitor BP (hypotension from loss of catecholamines), H'stix (rebound hypoglycaemia) | Sudden withdrawal of catecholamines → vasodilation + ↑insulin sensitivity |
| Crisis | ICU + IV phentolamine or nitroprusside | Immediate α-blockade |
First-line: usually either CBT or SSRIs with various self-help strategies [29]
| Treatment | Details | Mechanism |
|---|---|---|
| CBT | Targets fears of physical effects of anxiety → pointing out sequence of physical symptoms leading to fear → question patient's belief in feared outcome [29]; as effective as antidepressants [29] | Breaks the cognitive spiral: anxiety → somatic symptoms → catastrophic misinterpretation → more anxiety |
| SSRIs | First-line pharmacotherapy (e.g., sertraline, escitalopram); dose should be increased very slowly (initially ↑anxiety symptoms including palpitations) [29]; maintained for ≥6mo to prevent relapse [29] | ↑Serotonin in synaptic cleft → downregulates fear circuits in amygdala over weeks |
| SNRIs | Venlafaxine — alternative to SSRIs | Similar serotonergic mechanism + noradrenergic component |
| BZDs | Effective in controlling panic attacks when given at high doses; alprazolam commonly used [29]; but risk of dependence → generally avoided long-term | GABA-A receptor agonist → ↑Cl⁻ influx → neuronal inhibition → immediate anxiolysis |
| β-blockers | Low-dose propranolol PRN for situational anxiety with prominent somatic symptoms | Blocks peripheral β₁/β₂ effects of sympathetic activation (palpitations, tremor, sweating) without addressing the central anxiety |
Don't Just Sedate — Explain
For anxiety-related palpitations, the most powerful intervention is often a clear, compassionate explanation: "Your heart is structurally normal. What you're feeling is your body's stress response — adrenaline makes the heart beat faster and stronger. This is uncomfortable but not dangerous." This alone can reduce symptom severity significantly.
| Diagnosis | Acute Treatment | Long-Term Treatment |
|---|---|---|
| Ectopics (APB/VPB) | Reassurance; lifestyle (↓caffeine, alcohol, smoking) | β-blockers if symptomatic; ablation if burden > 10-15% |
| AVNRT/AVRT | Vagal manoeuvres → adenosine → cardioversion | Catheter ablation (curative, first-line); β-blockers/CCBs if decline ablation |
| AF | Rate control (BB/CCB/digoxin) or rhythm control (DCCV/drugs); anticoagulate | Long-term rate or rhythm control; PVI ablation; lifelong anticoagulation per CHA₂DS₂-VASc |
| AFL | Rate control or cardioversion | CTI ablation (first-line, > 95% success); anticoagulate |
| AT | BB/CCB; cardioversion if unstable | BB/CCB ± ablation ± amiodarone |
| MAT | Treat underlying cause; IV Mg | Correct electrolytes; treat lung/HF disease |
| VT (stable) | IV amiodarone/procainamide/sotalol; cardioversion | ICD ± antiarrhythmics ± ablation; treat underlying cause |
| VT/VF (pulseless) | Defibrillation + ACLS | ICD; ablation; optimise HF therapy |
| TdP | IV MgSO₄; stop offending drugs; overdrive pacing | Avoid QT-prolonging triggers; ICD if congenital LQTS |
| Bradycardia | Atropine → TCP/TVP | Permanent pacemaker if indicated |
| SSS | Atropine for acute pauses | Permanent pacemaker ± anticoagulation |
| WPW | Vagal/adenosine for AVRT; procainamide/cardioversion for pre-excited AF; NEVER AV nodal blockers for AF | Catheter ablation of accessory pathway |
| Sinus tachycardia | Treat underlying cause | Treat underlying cause |
| Anaemia | Transfusion if severe | Iron/B12/folate; investigate and treat cause |
| Thyrotoxicosis | β-blockers; antithyroid drugs | Definitive: RAI or thyroidectomy |
| Phaeochromocytoma | α-blockade → β-blockade | Surgery after adequate blockade |
| Anxiety/Panic | Reassurance; β-blockers PRN; BZDs short-term | CBT + SSRIs |
| Electrolyte | IV K⁺/Mg²⁺ replacement | Identify and correct underlying cause |
High Yield Summary
-
Unstable tachyarrhythmia → synchronised cardioversion (except sinus tachycardia — the only absolute C/I). Synchronisation avoids R-on-T → VF.
-
Unstable bradycardia → Atropine 0.5mg IV q3-5min (max 3mg) → TCP → TVP. Atropine won't work in denervated hearts or infranodal block.
-
SVT acute termination ladder: Vagal manoeuvres → Adenosine 6mg → 12mg → 12mg → IV BB/CCB → Cardioversion.
-
Adenosine: Rapid IV push (t½ < 10s). Diagnostic AND therapeutic. C/I in asthma and pre-excited AF.
-
AF management has 3 parallel streams: Rate control (BB/CCB/digoxin), Rhythm control (DCCV/drugs/ablation), Anticoagulation (CHA₂DS₂-VASc → DOACs).
-
Pre-excited AF (WPW) → NEVER give AV nodal blockers (digoxin, verapamil, diltiazem, adenosine). Use IV procainamide or cardioversion.
-
VT: Treat as VT until proven otherwise in wide complex tachycardia. Stable → amiodarone. Unstable/pulseless → defibrillation. Long-term → ICD.
-
TdP: IV MgSO₄ (regardless of serum Mg) + stop offending drugs + overdrive pacing.
-
Phaeochromocytoma: ALWAYS α-block before β-block. β-block alone → unopposed α → hypertensive crisis.
-
Panic disorder: CBT + SSRIs (start low, go slow). Never dismiss as "just anxiety" without excluding organic causes first.
-
Ectopics: Reassurance + lifestyle first. β-blockers if persistent. Ablation if burden > 10-15% (risk of tachycardia-mediated cardiomyopathy).
Active Recall - Palpitations Management
[1] Senior notes: Ryan Ho Cardiology.pdf (p61, Section 2.3 Palpitations) [2] Senior notes: Ryan Ho Fundamentals.pdf (p206, Section 3.1.3 Palpitations) [3] Lecture slides: murtagh merge.pdf (p72–74, Palpitations) [5] Senior notes: Ryan Ho Cardiology.pdf (p92, Focal and Multifocal Atrial Tachycardia) [9] Senior notes: Ryan Ho Endocrine.pdf (p66, Phaeochromocytoma) [13] Senior notes: Ryan Ho Critical Care.pdf (p28, Cardiac Arrest and ACLS) [14] Senior notes: Ryan Ho Cardiology.pdf (p83, Sick Sinus Syndrome) [15] Senior notes: Ryan Ho Endocrine.pdf (p94, Hypoglycaemia) [23] Senior notes: Ryan Ho Critical Care.pdf (p39, Management of Symptomatic Tachyarrhythmia) [24] Senior notes: Ryan Ho Cardiology.pdf (p88, Management of Bradyarrhythmias) [25] Senior notes: Ryan Ho Critical Care.pdf (p41, Management of Symptomatic Bradyarrhythmia) [26] Senior notes: Ryan Ho Cardiology.pdf (p139, Arrhythmia Management in MI) [27] Senior notes: felixlai.md (Beta-blocker pharmacology in thyrotoxicosis) [28] Senior notes: Ryan Ho Endocrine.pdf (p67, Phaeochromocytoma Management) [29] Senior notes: Ryan Ho Psychiatry.pdf (p181, Panic Disorder Management)
Complications of Palpitations and Their Underlying Causes
When we talk about "complications of palpitations," we are really discussing the complications of the underlying arrhythmias and conditions that produce the symptom. Palpitations themselves — the subjective awareness of the heartbeat — cannot directly harm a patient. But the arrhythmias and diseases behind them absolutely can. Think of it like this: the palpitation is the smoke alarm; the complications come from the fire.
The complications are best understood by grouping them according to the pathophysiological mechanism through which they cause harm.
This is the most feared complication and the reason we take palpitations seriously.
| Cause | Mechanism of SCD | Who Is at Risk |
|---|---|---|
| VT degenerating to VF [13] | Sustained VT → haemodynamic collapse → ischaemia → electrical instability → VF → no cardiac output → death. VF = totally uncoordinated contraction of ventricles [13] | Post-MI patients with myocardial scar, DCMP (LVEF ≤ 35%), HCMP, ARVC |
| WPW with AF [3] | Accessory pathway conducts AF impulses to ventricle without AV nodal delay → ventricular rate > 300 bpm → VF | WPW syndrome [3] — young, otherwise healthy patients |
| Torsades de Pointes (TdP) [3] | Prolonged QT → early afterdepolarisations → polymorphic VT → may self-terminate or degenerate to VF | Long QT syndrome [3], drugs that prolong QT, hypokalaemia, hypomagnesaemia [3] |
| Brugada syndrome | Na⁺ channel dysfunction → transmural voltage gradient → VF, typically during sleep or fever | Young Asian males (high prevalence in South-East Asia); palpitations or syncope may precede SCD |
| HCMP | Dynamic LVOT obstruction + disorganised myocardial architecture → VT/VF, especially during exertion | Typically during or after vigorous physical activity — most common cause of SCD in athletes < 35y |
Cardiac arrest causes: CAD (85%), structural heart disease (10%: AS, HCM, DCM, ARVD, congenital HD), Others (5%: LQTS, Brugada syndrome, WPWS, drug-induced TdP, severe electrolyte imbalance) [13]
Why this matters: A young patient presenting with exertional palpitations and a family history of sudden death under 40 is a medical emergency until you prove otherwise. The palpitation may be the only warning before a lethal arrhythmia.
SCD Prevention
Patients at high risk of SCD (survived VT/VF, LVEF ≤ 35% with HF, high-risk HCMP, high-risk channelopathy) require an implantable cardioverter-defibrillator (ICD). The ICD detects VT/VF and delivers an internal shock within seconds — this is the single most effective intervention for preventing SCD in high-risk patients.
The most clinically significant complication of atrial arrhythmias, especially atrial fibrillation [3].
Pathophysiology of AF-related stroke:
The left atrial appendage (LAA) is a muscular pouch in the left atrium. During normal sinus rhythm, the LAA contracts vigorously and empties with each heartbeat. In AF:
- Loss of coordinated atrial contraction → blood stasis in the LAA
- Virchow's triad activated: stasis (✓), endothelial injury (atrial remodelling ✓), hypercoagulable state (inflammatory mediators ✓)
- Thrombus forms in the LAA (90% of AF-related thrombi originate here)
- Embolisation → most commonly to the brain (MCA territory) → ischaemic stroke
| Complication | Arrhythmia | Magnitude of Risk | Mechanism |
|---|---|---|---|
| Ischaemic stroke | AF | 5-fold ↑ risk; AF accounts for 15-20% of all strokes | Thrombus from LAA → cerebral embolism. Strokes tend to be large and disabling because embolus occludes major vessels |
| Ischaemic stroke | AFL | Similar risk to AF | Same stasis mechanism; AFL often coexists with AF |
| Systemic embolism | AF | Renal, mesenteric, limb arteries | Same thrombotic source → any arterial territory |
| Paradoxical embolism | AF + PFO | Venous thrombus crosses PFO to arterial circulation | Patent foramen ovale creates right-to-left shunt, especially during Valsalva → venous emboli reach systemic circulation |
ECG for cardiac abnormalities (eg. AF) is part of the stroke workup [30] — because identifying AF changes management entirely (anticoagulation)
Prevention: Anticoagulation guided by CHA₂DS₂-VASc score. DOACs (dabigatran, rivaroxaban, apixaban, edoxaban) are preferred over warfarin for non-valvular AF. Left atrial appendage occlusion (e.g., Watchman device) for patients who cannot tolerate anticoagulation.
3. Heart Failure
Arrhythmias cause or exacerbate heart failure through multiple mechanisms.
This is a critically important and reversible complication.
Pathophysiology: Any sustained tachycardia (AF with fast ventricular rate, incessant SVT, frequent VPBs) → chronic ↑HR → ↑myocardial O₂ demand + ↓diastolic filling time + ↓coronary perfusion → myocardial energy depletion → progressive LV dilatation and systolic dysfunction → clinical HF.
Tachycardia-mediated cardiomyopathy is listed as a cause of DCMP — due to uncontrolled tachycardia [31]
Key features:
- The cardiomyopathy can develop from any sustained tachyarrhythmia, even seemingly benign ones like frequent VPBs ( > 10-15% burden)
- Reversible: LVEF can normalise completely after rate/rhythm control or ablation — this is why identifying and treating the arrhythmia is crucial
- Should be suspected whenever a patient presents with new HF + uncontrolled arrhythmia, especially if no other obvious HF aetiology
- AF causes HF through: (1) loss of atrial kick (contributes ~25% of CO; even more important in diastolic dysfunction), (2) irregularity itself ↓cardiac efficiency, (3) tachycardiomyopathy if rate uncontrolled
- HF causes AF through: atrial dilatation → atrial fibrosis → AF substrate → "AF begets HF begets AF" vicious cycle
- Severe bradycardia → ↓CO → forward failure (fatigue, syncope, renal impairment) + backward failure (congestion)
- Particularly in complete heart block with slow ventricular escape ( < 40 bpm)
Diastolic dysfunction: contributing factor in 80% of pts [32] ↓Compliance → ↓diastolic filling → ↑LV end-diastolic pressure → ↑pulmonary venous pressure → accounts for exertional dyspnoea [32]
When AF develops in HCMP (occurs in ~30%), the loss of atrial kick is catastrophic because the stiff, hypertrophied ventricle is highly dependent on active atrial contraction for filling → acute HF exacerbation.
Arrhythmias can cause syncope through ↓cerebral perfusion.
| Arrhythmia | Mechanism of Syncope |
|---|---|
| Sustained VT | Very rapid rate → ↓diastolic filling → ↓stroke volume → ↓CO → ↓cerebral perfusion |
| Complete heart block | Ventricular escape rate too slow ( < 40 bpm) to maintain adequate CO |
| Sick sinus syndrome (tachy-brady) [3] | During tachyarrhythmia, there is overdrive suppression of SA node → period of sinus arrest following termination of tachyarrhythmia [14] → the pause causes syncope |
| HCMP with dynamic LVOT obstruction | LVOT obstruction worsens with exertion → exertional syncope [32] |
| Pre-excited AF in WPW | Extremely rapid ventricular rate → ↓filling → ↓CO → syncope → may progress to VF |
| TdP | Self-terminating bursts → recurrent syncope; sustained → VF → cardiac arrest |
Why syncope during palpitations is a red flag: It implies that the arrhythmia is haemodynamically significant — the heart is failing to maintain cerebral perfusion. This dramatically increases the probability of a dangerous arrhythmia (VT, VF, high-degree block, pre-excited AF) and the risk of SCD.
Pathophysiology: Any sustained tachycardia ↑myocardial O₂ demand (↑HR → ↑contractility → ↑wall stress) while simultaneously ↓O₂ supply (↓diastolic time → ↓coronary perfusion time). If the patient has underlying coronary stenoses, this mismatch crosses a critical threshold → ischaemia.
Evolving phase of MI: associated arrhythmia because infarcted muscles are acidotic → K⁺ influx + Ca²⁺ efflux [17] — this creates a vicious cycle where ischaemia begets arrhythmia begets more ischaemia.
| Scenario | Mechanism |
|---|---|
| SVT or AF with fast rate in patient with CAD | Demand ischaemia → angina, ST changes, troponin rise (Type 2 MI) |
| VT in post-MI patient | VT ↓CO → ↓coronary perfusion → worsens ischaemia → VT becomes more refractory |
| Severe anaemia + tachycardia | Double hit: ↓O₂ carrying capacity + ↑demand → ischaemia even without CAD |
6. Complications Specific to Underlying Conditions Causing Palpitations
Phaeochromocytoma crisis: APO, ICH [10]
Symptoms of HTN complications: LV failure, MI and cardiomyopathy; Stroke or hypertensive retinopathy [9]
| Complication | Mechanism |
|---|---|
| Hypertensive crisis (including APO, ICH) | Massive catecholamine surge → extreme vasoconstriction → ↑↑afterload → flash pulmonary oedema; ↑↑BP → rupture of cerebral vessels → intracerebral haemorrhage |
| Catecholamine cardiomyopathy | Chronic catecholamine excess → direct myocardial toxicity (contraction band necrosis) → DCMP; mimics Takotsubo |
| Arrhythmias | Catecholamines ↑automaticity and triggered activity → sinus tachycardia, SVT, VT, VF |
| MI | Coronary vasospasm from α₁-stimulation + demand ischaemia from ↑HR/↑BP |
| Complication | Mechanism |
|---|---|
| AF (10-25% of thyrotoxic patients) | T3/T4 ↑β₁-receptor density + ↓atrial refractory period → facilitates AF |
| High-output heart failure | ↑CO + ↓SVR → volume overload → eventually LV decompensation |
| Angina / MI | ↑Myocardial O₂ demand (↑HR, ↑contractility) exceeds supply, especially with coexistent CAD |
| Thyroid storm | Life-threatening: fever, confusion, tachycardia, multi-organ failure; can cause fatal arrhythmia |
| Thyrotoxic periodic paralysis | ↑Na⁺/K⁺-ATPase → severe hypoK → arrhythmia risk + flaccid paralysis |
Hypokalaemia and hypomagnesaemia [3] are not just causes of palpitations — they are directly pro-arrhythmic:
| Level | ECG Changes | Arrhythmia Risk |
|---|---|---|
| K⁺ 3.0-3.5 mmol/L | ST depression, T-wave flattening, U waves | ↑Ectopics |
| K⁺ 2.5-3.0 mmol/L | Prominent U waves, T-U fusion | VT, AF |
| K⁺ < 2.5 mmol/L | Severe QT prolongation | VF, TdP, cardiac arrest |
| HyperK 6-7 mmol/L | Tall, peaked T waves [21] | |
| HyperK 8-10 mmol/L | Aberrant QRS complexes [21] | |
| HyperK 10-12 mmol/L | Ventricular fibrillation [21] | Cardiac arrest |
These are often underappreciated but clinically significant:
| Complication | Mechanism | Impact |
|---|---|---|
| Anxiety and health anxiety | Recurrent unpredictable palpitations → fear of cardiac death → catastrophic thinking | Avoidance behaviour, frequent A&E presentations, high healthcare utilisation |
| Agoraphobia | Panic attacks with palpitations → fear of attacks occurring in public → avoidance of open/public spaces | Social isolation, functional impairment |
| Depression [3] | Chronic anxiety + functional limitation from arrhythmia + medication side effects | 37% of panic disorder patients have lifetime major depression [6]; chronic AF patients have significantly ↑depression rates |
| Reduced quality of life | Symptoms (palpitations, syncope, fatigue) + medication side effects + lifestyle restrictions (exercise avoidance in LQTS/HCMP) | Impaired work capacity, social functioning, physical activity |
| Cardiac neurosis | Quite likely. Consider cardiac neurosis, anxiety [3] — once established, repeated reassurance often fails | Doctor-shopping, repeated investigations, iatrogenic harm from unnecessary procedures |
| Medication side effects | Amiodarone toxicity (thyroid, pulmonary fibrosis, hepatotoxicity, corneal deposits, photosensitivity); β-blocker fatigue/sexual dysfunction; anticoagulant bleeding | Can be as disabling as the arrhythmia itself |
Course of panic disorder: tends to be recurrent and chronic with fluctuating anxiety and depression. Impact: ↓QoL, functioning and ↑all-cause mortality (esp cardiovascular disorders) [33]
The Bidirectional Relationship Between Palpitations and Anxiety
Palpitations cause anxiety (fear of heart disease) and anxiety causes palpitations (sympathetic activation). This bidirectional loop can be extremely difficult to break and is the basis of panic disorder. Breaking it requires both medical reassurance (normal investigations) AND psychological intervention (CBT targeting catastrophic cognitions about bodily sensations).
The treatments for arrhythmias carry their own risks:
| Treatment | Complications | Mechanism |
|---|---|---|
| Anticoagulation (DOACs/warfarin) | Haemorrhage (GI, intracranial, other) | Impaired haemostasis |
| Amiodarone | Thyrotoxicosis or hypothyroidism; pulmonary fibrosis; hepatotoxicity; corneal microdeposits; peripheral neuropathy; photosensitivity (blue-grey skin) | Amiodarone is 37% iodine by weight → affects thyroid; accumulates in lipophilic tissues (lung, liver, cornea, skin) |
| Catheter ablation | Cardiac tamponade (perforation); pulmonary vein stenosis (after PVI); AV block (AVNRT ablation near AV node); stroke; phrenic nerve injury; oesophageal fistula (left atrial ablation) | Mechanical/thermal injury to adjacent structures |
| ICD | Inappropriate shocks (sinus tachycardia or AF misread as VT); lead fracture/infection; psychological impact of shocks; device-related endocarditis | Device algorithm errors; mechanical lead failure; foreign body infection |
| Pacemaker | Lead displacement; infection; pneumothorax (during insertion); pacemaker syndrome (AV dyssynchrony with VVI pacing); battery depletion | Procedural complications + long-term device limitations |
| Cardioversion | Thromboembolism (if inadequate pre-anticoagulation); skin burns; arrhythmia (VF if unsynchronised on T wave); transient myocardial stunning | Dislodgement of pre-existing LA thrombus; electrical injury |
| Antiarrhythmic drugs | Proarrhythmia — the greatest irony in arrhythmia management: drugs given to treat arrhythmias can cause new or worse arrhythmias | Class IC drugs (flecainide, propafenone) → ↑mortality in post-MI patients (CAST trial); Class III drugs → QT prolongation → TdP; digoxin toxicity → virtually any arrhythmia |
The Proarrhythmic Paradox
The CAST trial (1989) was a landmark study that showed flecainide and encainide (Class IC antiarrhythmics), given to suppress VPBs after MI, actually increased mortality by causing fatal VT/VF. This is why Class IC drugs are contraindicated in structural heart disease. It fundamentally changed how we prescribe antiarrhythmics — the principle is: never give flecainide or propafenone to anyone with structural heart disease or ischaemic heart disease.
| System | Complication | Most Commonly From | Mechanism |
|---|---|---|---|
| Cardiac — arrest | SCD from VF | VT, WPW+AF, TdP, LQTS, Brugada, HCMP | Degrades to VF → no output |
| Cardiac — failure | Tachycardiomyopathy | Any sustained tachycardia, high-burden VPBs | Chronic ↑HR → energy depletion → LV dilatation |
| Cardiac — ischaemia | Type 2 MI | Sustained tachycardia + underlying CAD | Supply-demand mismatch |
| Cerebrovascular | Stroke | AF, AFL | LA stasis → thrombus → embolism |
| Systemic embolic | Renal/mesenteric/limb ischaemia | AF | Same as stroke but to other territories |
| Neurological | Syncope, presyncope | VT, CHB, SSS, HCMP, TdP | ↓CO → ↓cerebral perfusion |
| Endocrine complications | Hypertensive crisis, catecholamine CMP | Phaeochromocytoma | Catecholamine surge |
| Psychological | Anxiety, depression, agoraphobia | Recurrent palpitations of any cause | Fear + avoidance cycle |
| Iatrogenic | Proarrhythmia, bleeding, device Cx | Treatment of arrhythmias | Drug/device-specific |
High Yield Summary
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Sudden cardiac death is the most feared complication — from VT/VF in structural HD, WPW+AF, TdP (LQTS/drugs/electrolytes), HCMP, Brugada. Prevention: ICD in high-risk patients.
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Stroke from AF — 5-fold increased risk. Thrombus forms in LAA due to stasis. Prevention: anticoagulation guided by CHA₂DS₂-VASc score.
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Tachycardiomyopathy — any sustained tachycardia (including "benign" VPBs at > 10% burden) can cause a reversible dilated cardiomyopathy. Identifying and treating the arrhythmia can normalise LVEF.
-
Syncope during palpitations = red flag → implies haemodynamically significant arrhythmia. Always warrants urgent evaluation.
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Type 2 MI — tachycardia → supply-demand mismatch → troponin rise, especially in patients with underlying CAD. This is not ACS but still dangerous.
-
Phaeochromocytoma crisis (APO, ICH) and thyroid storm are life-threatening complications of endocrine causes of palpitations.
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Electrolyte complications: HyperK follows a predictable ECG progression (peaked T → wide QRS → sine wave → VF). HypoK → prolonged QT → TdP.
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Proarrhythmia — antiarrhythmic drugs can paradoxically worsen arrhythmias. Class IC drugs (flecainide) are contraindicated in structural heart disease (CAST trial).
-
Psychological complications — recurrent palpitations cause anxiety, panic disorder, agoraphobia, depression, and cardiac neurosis. The palpitation-anxiety loop is bidirectional and requires both medical and psychological intervention.
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Treatment complications — amiodarone (thyroid/lung/liver/cornea), ablation (tamponade, PV stenosis), ICD (inappropriate shocks, infection), anticoagulation (bleeding).
Active Recall - Complications of Palpitations
References
[3] Lecture slides: murtagh merge.pdf (p72–74, Palpitations) [6] Senior notes: Ryan Ho Psychiatry.pdf (p178–179, Panic Disorder) [9] Senior notes: Ryan Ho Endocrine.pdf (p66, Phaeochromocytoma clinical features and complications) [10] Senior notes: maxim.md (Phaeochromocytoma section) [13] Senior notes: Ryan Ho Critical Care.pdf (p28, Cardiac Arrest causes) [14] Senior notes: Ryan Ho Cardiology.pdf (p83, Sick Sinus Syndrome) [17] Senior notes: Ryan Ho Cardiology.pdf (p127 and p139, MI definition and arrhythmia complications) [21] Senior notes: Ryan Ho Chemical Path.pdf (p14, Hyperkalaemia ECG changes) [30] Senior notes: Ryan Ho Neurology.pdf (p80, Stroke investigations including ECG for AF) [31] Senior notes: Ryan Ho Cardiology.pdf (p169, DCMP causes including tachycardia-mediated) [32] Senior notes: Ryan Ho Cardiology.pdf (p167, HCMP pathophysiology) [33] Senior notes: Ryan Ho Psychiatry.pdf (p179, Panic disorder course and prognosis)
High Yield Summary
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Definition: Palpitations = unexpected awareness of heartbeat. It is a symptom, not a diagnosis.
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Three mechanisms: (a) Tachyarrhythmias, (b) Hyperdynamic circulation exaggerating sinus rhythm, (c) Bradyarrhythmias with strong beats (↑diastolic filling → ↑stroke volume).
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Probability diagnosis (Murtagh): Anxiety, ectopics, sinus tachycardia, SVT, drugs/stimulants.
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Must not miss: MI, AF/AFL, VT, bradycardia/heart block, sick sinus syndrome, TdP, Long QT, WPW, hypoK/hypoMg, hypoglycaemia.
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Pitfalls often missed: Fever, pregnancy, menopause, caffeine/cocaine, mitral valve disease, AR, hypoxia.
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Masquerades: Depression, diabetes, drugs, anaemia, thyrotoxicosis, spinal dysfunction.
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Key history features: Character (tap it out!), onset/offset (sudden = re-entry, gradual = automaticity), triggers, termination (vagal manoeuvres = nodal re-entry), age, associated symptoms (syncope = red flag), drug/substance use, family history of SCD.
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Key examination: Usually normal between attacks. Check pulse (rate, rhythm, volume, character), look for anaemia, thyroid disease, anxiety, MVP, structural heart disease signs.
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HK-relevant aetiologies: AF (ageing population), TPP (young Asian males), HCMP (esp apical variant 25-30% in HK/Japan), phaeochromocytoma (5P's).
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Red flags: Syncope, exertional palpitations, FHx of SCD, structural heart disease, chest pain, abnormal ECG.
High Yield Summary
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Four DDx categories: (a) Tachyarrhythmias, (b) Hyperdynamic circulation, (c) Bradyarrhythmias, (d) Non-cardiac/functional.
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Most common causes: Anxiety, ectopics (APB/VPB), sinus tachycardia, SVT, drugs — these account for the vast majority of presentations.
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Must not miss: MI, AF/AFL, VT, heart block, SSS, TdP, LQTS, WPW, hypoK/hypoMg, hypoglycaemia.
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Bedside sorting: Get the patient to tap out the rhythm. Irregular = AF/MAT. Skip + pause = ectopics. Sudden rapid regular = re-entrant SVT. Gradual fast = sinus tachycardia. Slow heavy = bradycardia. Moderate regular + systemic symptoms = hyperdynamic state.
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Key DDx pair — anxiety vs AVNRT: Both common in young women. Sudden onset/offset + vagal termination = AVNRT. Gradual build-up with worry cascade = anxiety/panic. Never label palpitations as anxiety without at least one ECG.
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Thyrotoxicosis is the great imitator: Check TFTs even if clinical manifestations not apparent — can cause AF, sinus tachycardia, or TPP (in Asian males).
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WPW danger: Pre-excited AF can conduct rapidly → VF → SCD. Contraindication: AV nodal blockers (digoxin, verapamil, diltiazem) in known WPW with AF.
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HK-specific: AF (ageing), TPP (young Asian males), apical HCMP (25–30% of HK HCMP), RHD in older/immigrant patients.
High Yield Summary
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No formal diagnostic criteria for "palpitations" — the diagnosis is about identifying the underlying cause.
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12-lead ECG is the single most important first-line investigation. A normal ECG during symptoms essentially excludes arrhythmia. A normal ECG between episodes only excludes resting abnormalities (WPW pattern, prolonged QT, structural changes).
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Murtagh's investigation checklist: FBE, TFTs, serum glucose, U&E + Mg, ECG, cardiac enzymes, echocardiography, Holter monitoring.
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Ambulatory monitoring choice depends on symptom frequency: Daily → Holter; Weekly → extended Holter/event recorder; Monthly → external loop recorder; Very infrequent → ILR.
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The diagnostic correlation: Symptoms + arrhythmia simultaneously = diagnostic. Symptoms + normal rhythm = arrhythmia excluded. Arrhythmia + no symptoms = incidental finding.
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Always check TFTs — even in patients without obvious thyrotoxic features. Thyrotoxicosis is the great imitator and a common cause of AF.
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ECG red flags on resting ECG: Delta wave (WPW), prolonged QTc (LQTS/drugs/electrolytes), Brugada pattern, LVH (HCMP), epsilon waves (ARVC), Q waves (prior MI scar → VT substrate).
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Phaeochromocytoma: Biopsy is NEVER done. Diagnosis by 24h urine fractionated metanephrines (Sens 98%). Localise by CT/MRI + MIBG scan.
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Panic disorder diagnosis (DSM-5): Requires recurrent unexpected panic attacks with ≥4/13 symptoms + ≥1 month of worry/behavioural change + exclusion of organic causes + not better explained by another mental disorder.
High Yield Summary
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Unstable tachyarrhythmia → synchronised cardioversion (except sinus tachycardia — the only absolute C/I). Synchronisation avoids R-on-T → VF.
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Unstable bradycardia → Atropine 0.5mg IV q3-5min (max 3mg) → TCP → TVP. Atropine won't work in denervated hearts or infranodal block.
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SVT acute termination ladder: Vagal manoeuvres → Adenosine 6mg → 12mg → 12mg → IV BB/CCB → Cardioversion.
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Adenosine: Rapid IV push (t½ < 10s). Diagnostic AND therapeutic. C/I in asthma and pre-excited AF.
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AF management has 3 parallel streams: Rate control (BB/CCB/digoxin), Rhythm control (DCCV/drugs/ablation), Anticoagulation (CHA₂DS₂-VASc → DOACs).
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Pre-excited AF (WPW) → NEVER give AV nodal blockers (digoxin, verapamil, diltiazem, adenosine). Use IV procainamide or cardioversion.
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VT: Treat as VT until proven otherwise in wide complex tachycardia. Stable → amiodarone. Unstable/pulseless → defibrillation. Long-term → ICD.
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TdP: IV MgSO₄ (regardless of serum Mg) + stop offending drugs + overdrive pacing.
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Phaeochromocytoma: ALWAYS α-block before β-block. β-block alone → unopposed α → hypertensive crisis.
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Panic disorder: CBT + SSRIs (start low, go slow). Never dismiss as "just anxiety" without excluding organic causes first.
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Ectopics: Reassurance + lifestyle first. β-blockers if persistent. Ablation if burden > 10-15% (risk of tachycardia-mediated cardiomyopathy).
High Yield Summary
-
Sudden cardiac death is the most feared complication — from VT/VF in structural HD, WPW+AF, TdP (LQTS/drugs/electrolytes), HCMP, Brugada. Prevention: ICD in high-risk patients.
-
Stroke from AF — 5-fold increased risk. Thrombus forms in LAA due to stasis. Prevention: anticoagulation guided by CHA₂DS₂-VASc score.
-
Tachycardiomyopathy — any sustained tachycardia (including "benign" VPBs at > 10% burden) can cause a reversible dilated cardiomyopathy. Identifying and treating the arrhythmia can normalise LVEF.
-
Syncope during palpitations = red flag → implies haemodynamically significant arrhythmia. Always warrants urgent evaluation.
-
Type 2 MI — tachycardia → supply-demand mismatch → troponin rise, especially in patients with underlying CAD. This is not ACS but still dangerous.
-
Phaeochromocytoma crisis (APO, ICH) and thyroid storm are life-threatening complications of endocrine causes of palpitations.
-
Electrolyte complications: HyperK follows a predictable ECG progression (peaked T → wide QRS → sine wave → VF). HypoK → prolonged QT → TdP.
-
Proarrhythmia — antiarrhythmic drugs can paradoxically worsen arrhythmias. Class IC drugs (flecainide) are contraindicated in structural heart disease (CAST trial).
-
Psychological complications — recurrent palpitations cause anxiety, panic disorder, agoraphobia, depression, and cardiac neurosis. The palpitation-anxiety loop is bidirectional and requires both medical and psychological intervention.
-
Treatment complications — amiodarone (thyroid/lung/liver/cornea), ablation (tamponade, PV stenosis), ICD (inappropriate shocks, infection), anticoagulation (bleeding).
Oral/dental Pain/lesions
Oral/dental pain and lesions encompass a range of conditions affecting the teeth, gums, and oral mucosa—including caries, abscesses, gingivitis, aphthous ulcers, and mucosal lesions—that present with pain, swelling, or visible tissue changes.
Rectal Bleeding
Rectal bleeding is the passage of blood through the anus, originating from the rectum or lower gastrointestinal tract, which may indicate conditions ranging from hemorrhoids to colorectal malignancy.