Ventricular Arrhythmias

We cover atrial fibrillation in detail and devices separately. This page is the ventricular side — the half that matters most during exercise, because it is where an arrhythmia stops being a documentation point and becomes a reason to end the session.¹

Definition and classification

• Premature ventricular complexes (PVCs / ventricular ectopics) — single early beats of ventricular origin. Extremely common, including in healthy hearts.
• Non-sustained ventricular tachycardia (NSVT) — three or more consecutive ventricular beats at >100 bpm, lasting <30 seconds and self-terminating.
• Sustained ventricular tachycardia (VT) — ≥30 seconds, or requiring intervention sooner because of haemodynamic collapse. Monomorphic or polymorphic.
• Torsades de pointes — polymorphic VT on a background of QT prolongation.
• Ventricular fibrillation (VF) — disorganised activity with no effective output. Cardiac arrest.

Pathophysiology

Most sustained monomorphic VT is re-entrant, circulating around a fixed scar — typically post-infarct, or the fibrofatty replacement of arrhythmogenic cardiomyopathy. Polymorphic VT and VF more often reflect acute ischaemia, electrolyte disturbance or a channelopathy. Ectopy in a structurally normal heart is usually focal and benign. The distinction that matters clinically is not the rhythm's appearance but whether there is underlying structural heart disease, because that is what determines prognosis.^1,2

Co-morbidities

The company an arrhythmia keeps determines its seriousness. Ischaemic heart disease and prior infarction provide the scar that sustains most monomorphic VT. Heart failure with reduced ejection fraction is both a cause and a consequence — a high ectopic burden can itself impair function, and impaired function generates arrhythmia. Atrial fibrillation frequently coexists. Chronic kidney disease brings electrolyte instability; thyroid disease, obstructive sleep apnoea and obesity are all independently associated. ⚠ Sleep-disordered breathing is worth asking about directly, since nocturnal arrhythmia and untreated apnoea travel together and one is treatable.

Prevalence

Ventricular ectopy is extremely common: isolated PVCs are found in the majority of adults on prolonged ambulatory monitoring, and their frequency rises with age. Prevalence of the benign end is therefore near-universal, which is exactly why the finding alone means little. Sustained ventricular tachycardia is far less common and concentrated in structural heart disease. Sudden cardiac death accounts for a substantial share of all cardiovascular deaths, with ventricular arrhythmia the terminal mechanism in most; incidence rises steeply with age and with reduced ejection fraction, and inherited channelopathies account for a small but important minority in the young.²

Causes and contributors

Ischaemic heart disease and prior infarction; cardiomyopathies, particularly arrhythmogenic and hypertrophic phenotypes (see cardiomyopathies); heart failure with reduced ejection fraction; electrolyte disturbance, especially hypokalaemia and hypomagnesaemia; QT-prolonging drugs; inherited channelopathies such as long QT and Brugada syndromes; and, in athletic populations, occasionally no identifiable substrate at all.

Presentation

Palpitations, a sensation of a skipped or forceful beat, light-headedness, presyncope, syncope, chest discomfort or breathlessness. Syncope during exertion is a red flag and should never be attributed to a benign cause without cardiology assessment. Ectopy is frequently asymptomatic and found incidentally.

Investigation

Twelve-lead ECG; ambulatory monitoring to quantify ectopic burden; echocardiography for structural disease; exercise testing to reproduce exertional arrhythmia; cardiac MRI for scar and for arrhythmogenic phenotypes; electrophysiology study in selected cases. A PVC burden above roughly 10–15% on ambulatory monitoring raises the possibility of PVC-induced cardiomyopathy, which is reversible if the ectopy is suppressed or ablated.³

Medical management

Correct reversible causes first — ischaemia, electrolytes, offending drugs. Beta-blockers are first-line for symptomatic ectopy and for most VT prophylaxis. Amiodarone and other antiarrhythmics have a role but carry meaningful toxicity. Catheter ablation is effective for focal PVCs and for scar-related VT. Implantable cardioverter-defibrillators are indicated for secondary prevention after resuscitated arrest or haemodynamically significant VT, and for primary prevention in selected patients with reduced ejection fraction.^1,4

Medications

Beta-blockers are first-line for symptomatic ectopy and most VT prophylaxis, and are the agent least likely to cause harm. Amiodarone is effective but carries thyroid, hepatic, pulmonary and ocular toxicity with cumulative dose — ⚠ amiodarone pulmonary toxicity is a genuine differential for new breathlessness in a cardiac patient and is easily attributed to heart failure instead. Class I agents are largely avoided in structural disease after the CAST experience showed increased mortality despite effective ectopy suppression. Sotalol and mexiletine have defined niches. Correcting potassium and magnesium is treatment, not housekeeping. ⏹ For us: nearly all of these blunt the heart-rate response, so prescription runs on workload and Borg — see prescribing exercise from test results.

Multi-system manifestations

Inherited arrhythmia syndromes are systemic and familial. Arrhythmogenic cardiomyopathy may involve skin and hair in some variants; some channelopathies carry sensorineural deafness or seizure phenotypes, and epilepsy is a recognised misdiagnosis of arrhythmic syncope. Sarcoidosis and amyloidosis both cause arrhythmia with extracardiac disease — sarcoid affecting the lungs is directly relevant to a cardiorespiratory service. ⏹ A familial diagnosis has implications for relatives, and patients frequently carry the weight of that; family screening is standard where an inherited cause is identified.

Warning signs

Living with a ventricular arrhythmia

The lived problem is usually fear rather than the rhythm. Palpitations are frightening, and after an ICD shock many people restrict activity drastically — the shock is painful, unpredictable, and remembered. Anxiety and avoidance limit function more often than the arrhythmia does, and this is where a supervised programme earns its place: successful graded exertion is itself the treatment for the fear. Practical matters that need answering honestly: driving restrictions, which vary with diagnosis and device and are set by regulation; return to work; whether sex and sport are safe; and what to do if the device fires. Device recipients also carry a small but real burden of electromagnetic-interference caution.

Prognosis

Prognosis tracks the substrate, not the trace. Frequent ectopy in a structurally normal heart carries a good outlook, and reassurance is appropriate.³ The same ectopy with prior infarction, reduced ejection fraction or an arrhythmogenic phenotype carries real risk of sudden death.^1,2 ICDs improve survival in appropriately selected patients, and ablation reduces recurrence and shock burden in scar-related VT. PVC-induced cardiomyopathy is genuinely reversible when the ectopy is suppressed — one of the more satisfying outcomes in the field. Exercise-based cardiac rehabilitation reduces cardiovascular mortality in the coronary disease that underlies most of this.⁶

Exercise, monitoring and what stops a session

This is the practical core for a rehabilitation service. Exercise-induced ectopy that suppresses as heart rate rises is generally benign; ectopy that increases with exertion, or appears in recovery, warrants review.⁵

These are conventional thresholds for a supervised programme and should be read alongside local policy and any individualised limits set by the treating cardiologist, which take precedence.

Patients with an ICD

Know the programmed therapy zone — the heart rate at which the device will deliver a shock — and prescribe training with a clear margin below it, conventionally at least 20 bpm. See pacemakers and ICDs for device-specific considerations, including upper-limb restrictions after implantation.

Role of the physiotherapist

Deliver supervised cardiac rehabilitation with rhythm and symptom monitoring; recognise the thresholds above and act on them without hesitation; maintain resuscitation competence, because this is one of the few outpatient settings where VF is a realistic event; and address the anxiety that frequently follows an arrhythmia or an ICD shock, which limits activity more often than the arrhythmia itself does. Familiarity with ECG basics is assumed.

Part 1 · References

1. Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J 2022;43(40):3997–4126.
2. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation 2018;138(13):e272–e391.
3. Baman TS, Lange DC, Ilg KJ, et al. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm 2010;7(7):865–869.
4. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J 2015;36(41):2793–2867.
5. Frolkis JP, Pothier CE, Blackstone EH, Lauer MS. Frequent ventricular ectopy after exercise as a predictor of death. N Engl J Med 2003;348(9):781–790.
6. Pelliccia A, Sharma S, Gati S, et al. 2020 ESC guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42(1):17–96.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.