Palpitations
- Differential
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- Arrhythmias – AF/flutter, AVNRT, AVRT, ectopics, sick sinus syndrome, heart block, ventricular arrhythmias, PPM/ICD anomalies
- Drugs
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- Caffeine, nicotine, recreational drugs and ETOH
- For respiratory disease – salbutamol, ipratropium, theophylline, nasal pseudoephedrine
- For CV disease – hydralazine, digoxin, flecainide, betablocker withdrawal
- Any drugs that prolong the QTC including some antibiotics, antipsychotics and antidepressants
- Steroids
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- Structural heart disease – valvular HD, congenital HD, HCM, HF, RV strain from PE
- Endocrine – thyrotoxicosis, hypoglycaemia
- Infection/fever
- Anaemia and dehydration
- Postural hypotension, vasovagal episodes and POTS
- Menopause and pregnancy
- Anxiety / depression / stress / panic attacks
- Rarer causes – pheochromocytoma, carcinoid, Pagets
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- Often difficult to find a cause. Up to 30% diagnosed initially with anxiety, and half of these will get a different diagnosis 3 years later
- Ask about
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- Triggers – ETOH, drugs (incl over the counter and recreational), situations, stress
- Frequency / duration / onset
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- Sudden onset more likely SVT, gradual more likely atrial tachycardia.
- Ask about the feeling of missed beats
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- Red flags – exercise-associated, syncope, chest pain, SOB, family hx of SCD (in such cases discuss with cardiology)
- Symptoms of associated conditions eg thyrotoxicosis, OSA, infection, GI bleeding
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- Clues to diagnosis
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- If fear and bradycardia – very often an underlying cardiac cause
- AVRT becomes less common with increasing age. AF and AVNRT become more common
- Wearable tech – eg watches with ECG function can be useful
- Atrial tachycardia is suggested by grouped fast beats, loss of diurnal variation in heart rate, abnormal p wave axis/inverted Ps, feeling of missed beats
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- ECG. Assess for
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- PR interval (WPW, heart block)
- Atrial or ventricular arrhythmias
- Ectopics
- QTC duration
- Evidence of old/current ischaemia, or ventricular hypertrophy
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- Driving
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- If an arrhythmia has caused incapacity (syncope or pre-syncope) – patient must not drive and should usually inform the DVLA (especially if symptoms remain uncontrolled)
- Can restart after one month if cause identified and symptoms controlled
- More rules apply if patient has an ICD or class 2 license
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- Investigations to consider
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- Bloods incl CRP, TFTs, Hb, HbA1c, d-dimer, bone profile, magnesium
- Prospective event monitoring
- Wearable devices
- Holter (not particularly useful if symptoms infrequent. Can be useful if ectopics on ECG to establish burden)
- Echo if murmur, suspcted structural HD or HF, >10% burden of ventricular ectopics
- See Cardiological investigations
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Ectopy
- Atrial ectopics (PACs).
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- >500 PACs (atrial ectopics) in 24 hours = high burden
- PACs are not benign (high burden have 2 x stroke risk without AF) and increases risk of later developing AF (due to a type of atrial cardiomyopathy)
- Probability of AF: if >100 PACs, <9% risk, if >1500 PACs 40% risk
- Do CHA2DS2-VASc score (imagine if they did develop AF) in order to decide what to do / how to manage risk factors / follow up
- Can treat with betablockers – bisoprolol, propranolol, nebivolol (or just reassure, depending on how symptomatic)
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- Ventricular ectopics (VEs / PVCs)
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- Early and often wide QRS without preceding Q wave
- Can be asymptomatic, or cause chest discomfort, skipped beat sensation, SOB, fatigue, pre-syncope. Can be symptomatic at any burden
- Usually benign unless family hx of SCD
- Common – at least 1 PVC occurs in 70% of people in 24 hours
- Origin
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- Can originate in areas of myocardial fibrosis (although this isn’t particularly important, more important to know if heart is structurally normal or not).
- Multifocal PVCs or those with non-outflow tract origins, are perhaps more concerning though
- RV outflow tract PVCs are often amenable to ablation (but can also be a an early manifestation of ARVC)
- RVOT PVCs tend to be positive in the inferior leads and I, with LBBB morphology.
- LV originating PVCs are riskier to treat with ablation
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- Complications / associations
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- PVC-induced cardiomyopathy (most cases occur when burden is >10%, and higher risk when burden >20%). Can be hard to tell if PVC is a symptom or cause of LV dysfunction (consider time course and CMR findings)
- PVC-triggered malignant ventricular arrythmias (rare)
- increased incidence of AF and heart failure with PVC rates burden > 0.8%
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- Assess for
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- Family hx of SCD, cardiac devices, cardiomyopathy
- Severity of symptoms if present
- Hx of syncope
- Impaired LV on last echo (more likely to treat in this instance). Get up to date echo for everyone
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- CMR for some (and always for those with PVC burdens >10% with reduced LVEF not explained by underlying heart disease, or anyone with burden >20%, or if suspicion of cardiomyopathy)
- Burden
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- A few are normal (probably ok if <5%). Might discuss with cardio if 5-10% in a young patient. Usually can discharge if burden <10% and no symptoms.
- >10% is significant. This increases risk of LV dysfunction. So discuss with cardio.
- >20% is associated with developing a cardiomyopathy / HF. Needs regular echo and most get suppression therapy regardless of symptoms
- No clear consensus on normal burden but >500 in 24 hours is not normal
- Non-sustained VT is 3 or more consecutive beats at a rate of >100 with duration of <30s. Non-sustained VT can be normal, but do an echo. Discuss NSVT with cardio unless there’s an obvious cause and plan in place (eg previous MI)
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- Treatment
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- Reassurance if low symptom burden, normal EF and low burden
- Pursue PVC suppression if bothersome symptoms or low EF – betablockers 1st Sometimes then repeat holter to assess impact on burden
- Can sometimes use CCBs, sotalol, amioderone or flecainide
- Ablation can be done – usually for RV outflow tract ectopy (ie LBBB / negative morphology of ectopic beats in chest leads and positive beats in inferior leads). 2-5% complication rate (vascular access issues, tamponade, AV block, stroke). Success rate around 85%.
- Serveillance echo for anyone with burden >10% and no LV dysfunction.
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