Atrial Flutter

Cavotricuspid Isthmus–Dependent

• Typical atrial flutter is defined as a macro–re-entrant atrial tachycardia with atrial rates generally between 250 and 320 beats per minute.
• The arrhythmia is sustained by a re-entry circuit in the right atrium, critically dependent on the cavotricuspid isthmus (CTI). The CTI lies between the tricuspid annulus anteriorly and the crista terminalis/eustachian ridge posteriorly, with the right atrial endocardial cavity forming the remaining pathway.

Anticlockwise Type

• In the anticlockwise form, when viewed en face at the tricuspid annulus, electrical activation travels up the interatrial septum and then down the right atrial free wall, completing a counterclockwise circuit.
• The electrocardiographic hallmark is the presence of continuous saw-tooth flutter waves (F waves):
  • Negative deflections in the inferior leads (II, III, aVF).
  • Positive deflections in lead V1.
• The ventricular response most commonly demonstrates 2:1 atrioventricular conduction, producing a ventricular rate of around 150 beats per minute, although other ratios (3:1, 4:1) may occur.
• This arrhythmia represents organised atrial activation, with large portions of the right atrium involved in the re-entrant circuit. It is distinct from atrial fibrillation, but both arrhythmias often coexist or alternate in the same patient.

Structural atrial abnormalities

Atrial dilation

• Atrial dilation is a frequent substrate, often arising from chronic pressure or volume overload due to conditions such as valvular heart disease, myocardial infarction, pulmonary embolism, or cardiomyopathy.
• Dilation facilitates re-entry by lengthening conduction pathways and promoting heterogeneity of conduction.

Incisional scars

• Incisional scars from prior atrial surgery, particularly procedures for congenital heart disease or valve repair, may create anatomic barriers that form part of re-entrant circuits.

Ablation-related scarring

• Ablation-related scarring following procedures for atrial fibrillation can promote atypical flutter circuits, especially when ablation lines are incomplete.

Idiopathic atrial fibrosis

• Idiopathic atrial fibrosis, developing with ageing or in the absence of other disease, may also serve as a substrate.

Cardiac disorders

• Coronary artery disease and hypertensive heart disease are frequently observed in patients with atrial flutter, each accounting for approximately one third of cases.
• Rheumatic heart disease, congenital structural defects, and pericarditis are established associations.
• Less commonly, atrial flutter has been reported in the setting of mitral valve prolapse or acute myocardial infarction.

Metabolic and systemic contributors

• Thyrotoxicosis, alcohol consumption, and pericarditis are recognised precipitants.
• Electrolyte disturbances (such as hypokalaemia or hypomagnesaemia) may create conduction heterogeneity favouring re-entry.
• Diabetes, obesity, and pheochromocytoma have been linked with increased risk.

Respiratory disease

• Chronic obstructive pulmonary disease, asthma, pneumonia, and hypoxia can trigger atrial flutter, often in conjunction with atrial fibrillation.
• Pulmonary embolism may act as a precipitant through acute right atrial strain and hypoxaemia.

Pharmacological triggers

• Anti-arrhythmic therapy for atrial fibrillation can paradoxically induce atrial flutter. This phenomenon is most commonly observed with Vaughan Williams class Ic drugs (flecainide, propafenone) and amiodarone.
• Digitalis toxicity, though rare, has also been implicated.

Surgical and procedural associations

• Open heart surgery may result in macro–re-entrant atrial tachycardia due to natural barriers, atriotomy scars, or prosthetic materials.
• Pulmonary vein isolation procedures for atrial fibrillation may promote atypical left atrial flutter, especially where ablation lines are incomplete.

Genetic predisposition

• Genome-wide association studies have demonstrated genetic susceptibility.
• The PITX2 gene (chromosome locus 4q25), which governs left–right cardiac asymmetry, has shown strong associations with atrial fibrillation and an even greater association with typical atrial flutter.
• No clinical genetic test is yet available to stratify risk.

Electrophysiological basis

• Atrial flutter requires the presence of a re-entry circuit consisting of pathways with different conduction velocities, heterogeneous refractory periods across atrial tissue, and a functional central core around which the re-entrant wavefront circulates.
• In typical cavotricuspid isthmus–dependent flutter, initiation often follows an ectopic beat that depolarises one segment of the circuit while adjacent tissue remains excitable, perpetuating the tachycardia.

Typical atrial flutter

• The commonest form of atrial flutter is a macro–re-entrant tachycardia involving a single circuit in the right atrium, most often circulating counterclockwise around the tricuspid valve annulus.
• The critical zone for conduction is the cavotricuspid isthmus (CTI), situated between the tricuspid valve annulus and the coronary sinus ostium. This region provides a pathway of slow conduction, which sustains the circuit.
• The anatomical boundaries of the re-entry loop are formed by the tricuspid annulus, crista terminalis, eustachian ridge, inferior vena cava, and coronary sinus os. The Todaro tendon contributes to delineating the circuit.
• Crista terminalis acts as a functional conduction barrier, enforcing transverse block and permitting the circuit to persist.
• Conduction typically proceeds up the interatrial septum and down the right atrial free wall, producing the classical counterclockwise activation sequence.
• On the ECG, this manifests as negative flutter waves in leads II, III, aVF and positive flutter waves in lead V1.
• Less frequently, the circuit may propagate in the reverse (clockwise) direction, giving rise to reverse typical atrial flutter, where ECG waveforms are inverted compared with the counterclockwise pattern.
• Atrial activation occurs continuously, without an isoelectric baseline between flutter waves, and atrioventricular conduction is usually 2:1, producing a ventricular rate around 150 bpm. However, conduction ratios may vary depending on atrioventricular nodal refractoriness and autonomic tone.

Electrophysiological mechanisms

• Sustained flutter requires:
  • Coexistent zones of fast and slow conduction.
  • Differences in refractory periods across atrial tissue.
  • A functional central core (bounded by fixed or functional barriers) that allows the re-entrant wavefront to circulate.
• The excitable gap within the circuit enables entrainment, a feature exploited in electrophysiological studies to characterise flutter mechanisms.
• Structural changes such as fibrosis from ageing or atrial dilation can exacerbate conduction heterogeneity, facilitating circuit stability. Low-voltage areas in the CTI or crista terminalis are markers of arrhythmogenic substrate.

Atypical atrial flutter

• Atypical flutter encompasses circuits not dependent on the CTI. These may originate in either atrium and often involve scar tissue or regions of low-voltage conduction.
• Right atrial atypical circuits may arise from surgical scars, the superior vena cava, or the terminal crest.
• Left atrial atypical flutter often follows interventions such as pulmonary vein isolation or atriotomy, with circuits involving the mitral annulus or atriotomy lines.
• Fibrosis due to chronic raised atrial pressures or cardiomyopathy may create low-voltage substrates that sustain these circuits.
• These arrhythmias are frequently challenging to diagnose on ECG alone, as their flutter wave morphology does not conform to the criteria of typical or reverse typical flutter. Electrophysiological mapping is required to localise and ablate the circuit.
• Success rates of ablation are lower in intra-atrial septal macro-reentry than in free-wall tachycardias.

Experimental and anatomical insights

• Animal models demonstrate that blocks between the superior and inferior vena cava, mimicking the human crista terminalis, are essential for maintaining flutter.
• These models highlight how anatomical and functional barriers combine to permit macroreentry.
• Electroanatomic mapping in humans confirms these pathways, demonstrating caudocranial septal activation during counterclockwise flutter and reversed sequences in clockwise circuits.

Incidence and prevalence

• Atrial flutter is the second most common sustained cardiac arrhythmia after atrial fibrillation.
• Its incidence in large population studies is approximately 88 per 100,000 person-years, translating to around 200,000 new cases per year in the United States.
• The condition is substantially less frequent than atrial fibrillation, which accounts for the majority of supraventricular tachycardia admissions, while atrial flutter represents about 10% of such cases.
• The risk of atrial flutter increases steeply with age, from 5 per 100,000 in individuals younger than 50 years to nearly 600 per 100,000 in those older than 80 years.

Age and sex distribution

• Atrial flutter is predominantly a disorder of older adults, with a mean age of presentation around 64 years in clinical series.
• The arrhythmia is 2.5 times more common in men than women, with some studies reporting male predominance as high as 75% of cases.
• The prevalence of atrial flutter parallels that of atrial fibrillation, increasing markedly with advancing age.

Relationship with atrial fibrillation

• Atrial fibrillation and atrial flutter often coexist.
• Prior to ablation, 24% to 62% of patients with atrial flutter also have atrial fibrillation; after ablation, the proportion rises to 30% to 70%.
• Both arrhythmias share overlapping risk factors, and atrial flutter may act as a transitional or alternate rhythm in patients with atrial fibrillation.

Associated conditions and comorbidities

• More than 98% of cases are linked to an identifiable comorbidity or predisposing condition.
• Common associations include chronic obstructive pulmonary disease, pulmonary hypertension, and heart failure.
• Isolated atrial flutter without structural heart disease is rare, usually appearing only when atrial dilation or remodelling has occurred.
• Other risk factors mirror those for atrial fibrillation, including systemic hypertension, diabetes mellitus, obesity, and chronic alcohol use.

Typical presenting symptoms

Palpitations

• The most common complaint, reflecting rapid atrial activity and ventricular conduction.

Fatigue, exercise intolerance, and lightheadedness

• Frequent symptoms resulting from reduced cardiac output.

Dyspnoea

• May occur on exertion or at rest, reflecting impaired filling or coexistent pulmonary disease.

Presyncope or syncope

• Can appear in patients with poor haemodynamic reserve or those who develop very rapid ventricular rates.

Chest pain or angina

• Occurs when myocardial oxygen demand exceeds supply, particularly in those with underlying ischaemic heart disease.

Less common presentations

• Severe dyspnoea, hypotension, or anxiety may indicate haemodynamic compromise.

Thromboembolic and ischaemic complications

Systemic embolic events

• Atrial flutter can precipitate stroke or peripheral embolism, though this is less common at first presentation.

Pulmonary embolism or myocardial ischaemia

• Patients may report symptoms related to these, either as consequences of atrial flutter or as precipitating factors.

Associated or precipitating conditions

Cardiac or thoracic procedures

• Past interventions such as open-heart surgery, atrial septal defect repair, or prior ablation can leave atrial scars acting as substrates.

Recent illnesses

• Pneumonia, pulmonary embolism, or decompensated heart failure may trigger atrial flutter.

Medical comorbidities

• Hyperthyroidism, chronic obstructive pulmonary disease, asthma, diabetes, or hypertension are frequent associations.

Substance and drug use

• Alcohol excess is a recognised precipitant.
• Stimulants such as cocaine, methamphetamine, ginseng, and ephedra may provoke episodes.

Medication history

• Class Ic anti-arrhythmic agents (flecainide, propafenone), amiodarone, and digitalis toxicity are important to identify as potential triggers.

Temporal characteristics

Onset, duration, and frequency

• These should be established, as they influence management decisions.

Duration beyond 48 hours

• Carries an increased risk of left atrial thrombus; anticoagulation or transoesophageal echocardiography is required before cardioversion.

Termination pattern

• Patients may report whether flutter episodes resolve spontaneously or require intervention.

Special considerations

Wolff–Parkinson–White syndrome

• These patients are at risk of 1:1 atrioventricular conduction, potentially causing ventricular fibrillation; a history of pre-excitation should be elicited.

Alcohol-related atrial flutter with reduced ejection fraction

• Heavy alcohol intake is often reported, with a high prevalence of left atrial appendage thrombus.

Alternation with atrial fibrillation

• Many patients describe atrial flutter as unstable over time, alternating with atrial fibrillation or reverting to sinus rhythm.

General assessment and vital signs

Heart rate

• Often close to 150 beats/min due to 2:1 atrioventricular block, though variability in block may result in slightly irregular or higher rates.

Blood pressure

• Usually preserved, but hypotension can occur in unstable cases, particularly with rapid ventricular response.

Oxygen saturation

• Should be checked, as hypoxaemia may accompany decompensated cardiac or pulmonary disease.

General appearance

• Diaphoresis or acute dyspnoea may indicate haemodynamic compromise.
• Overall patient appearance helps determine urgency of rhythm restoration.

Cardiovascular findings

Pulse

• May be regular or irregularly regular, depending on the atrioventricular conduction ratio.

Jugular venous pulsations

• Can reveal rapid flutter waves or “cannon a waves”, reflecting atrial contraction against closed atrioventricular valves.

Heart sounds

• Auscultation may demonstrate:
  • An irregular rhythm.
  • Extra heart sounds or a gallop rhythm, indicating reduced compliance or volume overload.
  • Murmurs pointing to concurrent valvular disease (e.g., mitral or tricuspid regurgitation).

Point of maximal impulse (PMI)

• May be displaced or forceful in patients with underlying ventricular dysfunction.

Respiratory findings

Lung auscultation

• Crackles or rales may indicate pulmonary congestion secondary to left-sided heart failure.
• Tachypnoea can accompany decompensated heart failure or pulmonary comorbidities.

Peripheral signs

Oedema and perfusion

• Lower limb oedema or impaired peripheral perfusion may reflect systemic venous congestion or right-sided failure.

Abdominal findings

• Abdominal distension or hepatomegaly may be observed in chronic right-sided involvement.

Neurological and embolic manifestations

Neurological deficit

• Stroke or transient ischaemic attack may be evident if systemic embolisation has occurred.

Peripheral embolism

• Signs of limb ischaemia or other embolic events can occasionally be detected.

Complications evident on examination

Heart failure

• Pulmonary oedema, raised jugular venous pressure, and peripheral oedema may complicate atrial flutter.

Myocardial ischaemia

• Chest pain with tachyarrhythmia may suggest demand ischaemia.

Severe bradycardia

• Occasionally complicates atrial flutter, especially with drug therapy or conduction disease.

Approach considerations

• Electrocardiography (ECG) is the cornerstone of diagnosis, allowing distinction between typical and atypical flutter.
• Transthoracic echocardiography (TTE) is the preferred first-line imaging study.
• Laboratory studies should be directed by history and examination.

Thyroid function tests

• Indicated to exclude hyperthyroidism, a reversible but uncommon cause of atrial flutter.

Full blood count

• Ordered if anaemia is suspected or there is a history of recent blood loss.

Renal function and serum electrolytes

• Evaluates imbalances that may contribute to arrhythmogenesis and to guide safe medical therapy.

Pulmonary function tests

• Considered when chronic lung disease is suspected as a precipitant.

Drug levels

• Measurement of serum digoxin levels is useful when digitalis toxicity is suspected.

Additional testing

• High-sensitivity troponin if myocardial infarction is suspected.
• Arterial blood gases may be used in cases of hypoxia or carbon monoxide exposure.
• CT pulmonary angiography should be performed when pulmonary embolism is clinically suspected.

Chest radiography

• Frequently normal in atrial flutter.
• May demonstrate pulmonary oedema in decompensated cases or signs of underlying pulmonary disease.

Electrocardiography

Typical findings

• Saw-tooth flutter waves (F waves) in leads II, III, aVF; positive in V1 during counterclockwise circuits.
• Atrial rate usually 250–350 bpm (typical flutter) or 350–450 bpm (atypical flutter).
• Ventricular response most often 150 bpm due to 2:1 block, but ratios of 3:1 or 4:1 also occur.
• Reverse typical flutter (clockwise) shows upright flutter waves in the inferior leads with negative V1.
• Flutter waves may distort the ST–T segments, occasionally mimicking ischaemia.

Predictive value of morphology

• Negative inferior flutter waves with positive V1 strongly suggest counterclockwise re-entry.
• Positive inferior flutter waves with negative V1 are consistent with clockwise or atypical re-entry.

Diagnostic aids

Vagal manoeuvres

• Carotid sinus massage or Valsalva may transiently increase AV block and expose flutter waves.

Adenosine

• IV administration can help confirm diagnosis by producing transient AV nodal block.
• May rarely cause 1:1 AV conduction or induce atrial fibrillation; should only be used with monitoring.

Ambulatory monitoring

• Holter or event recorders help confirm intermittent arrhythmias, define triggers, and assess rate control.

Exercise testing

• Can unmask exercise-induced flutter or atrial fibrillation.
• Also assists in evaluation of concomitant ischaemic heart disease.

Echocardiography

Transthoracic echocardiography (TTE)

• Baseline evaluation of atrial and ventricular size and function.
• Detects valvular or pericardial pathology.
• Provides right ventricular systolic pressures to assess for pulmonary hypertension.

Transoesophageal echocardiography (TEE)

• Preferred test for detecting left atrial thrombus, particularly before cardioversion.
• More sensitive than TTE for identifying left atrial appendage thrombus.

Further investigations

Electrophysiological studies

• Used when ablation is being considered or when diagnosis is uncertain.
• Allows direct mapping of re-entrant circuits.

Atrial electrogram

• May assist when surface ECG is inconclusive, though rarely necessary in practice.

Atrial fibrillation

• Defined by the absence of organised atrial activity and replacement with fibrillatory waves of variable morphology, amplitude, and timing.
• The ventricular rhythm is irregularly irregular, with no consistent atrial-to-ventricular conduction ratio.
• In contrast to atrial flutter, there are no continuous saw-tooth F waves.

Atrial tachycardia

• Can mimic flutter, especially when associated with AV block.
• ECG shows discrete P waves with isoelectric intervals between them, distinguishing it from the continuous activity of flutter.
• At high atrial rates, separation from atypical flutter may be challenging without electrophysiological mapping.

Multifocal atrial tachycardia

• Characterised by at least three distinct P-wave morphologies with variable atrial cycle length.
• The ventricular rhythm is irregular, and isoelectric baselines are visible between atrial deflections.
• Strongly associated with chronic lung disease, particularly chronic obstructive pulmonary disease.

ECG artefact

• Tremor, shivering, or electrode interference may generate apparent flutter-like waves.
• These do not demonstrate consistent atrial-ventricular relationships and often vary with movement, helping distinguish them from true atrial flutter.

Diagnostic confirmation

• In most patients, a 12-lead ECG suffices for differentiation.
• When uncertainty remains, particularly before intervention, electrophysiology studies can provide definitive diagnosis and mapping.

Haemodynamically unstable patients

Supportive measures

• Administer controlled oxygen therapy (SpO₂ 94–96% in most, 88–92% if risk of hypercapnic respiratory failure).
• Continuous ECG and blood pressure monitoring.
• Secure intravenous access.
• Identify and correct reversible precipitants such as electrolyte imbalance.

Emergency electrical cardioversion

• Immediate synchronised DC cardioversion is the treatment of choice.
• First shock: 70–120 J biphasic.
• Repeat with stepwise escalation up to three shocks if needed.
• Provide sedation or anaesthetic support in conscious patients.
• Seek urgent cardiology input if cardioversion fails after three shocks.

Haemodynamically stable patients

Rate control

• Begin with AV nodal blocking drugs:
  • Beta-blockers (avoid in decompensated heart failure).
  • Non-dihydropyridine calcium channel blockers (verapamil, diltiazem – avoid in hypotension or reduced ejection fraction).
  • Digoxin may be used, particularly if flutter converts to atrial fibrillation.
• Contraindicated in pre-excitation syndromes such as Wolff–Parkinson–White.
• Often difficult to achieve adequate rate control; restoration of sinus rhythm is usually preferred.

Rhythm control: electrical cardioversion

• Electrical cardioversion is highly effective (95–100% success at low-energy shocks).
• Recommended if onset <48 hours, or guided by TEE when >48 hours or uncertain.
• Should be considered in symptomatic patients or those eligible for ablation.

Rhythm control: pharmacological cardioversion

• Less effective than electrical cardioversion and associated with proarrhythmia.
• Consider only when electrical cardioversion is unavailable or declined.
• Options include flecainide (with AV nodal blocker), amiodarone, or ibutilide (not UK-licensed).
• Continuous ECG monitoring is required during administration.

Recurrent or refractory atrial flutter

Catheter ablation

• First-line definitive therapy for cavotricuspid isthmus–dependent flutter.
• Indicated for symptomatic, recurrent, or pharmacologically refractory flutter, or if tachycardiomyopathy is present.
• Success rates exceed 90% with low recurrence.
• Recommended by ESC and ACC/AHA/HRS guidelines as the treatment of choice in suitable candidates.

Long-term drug therapy

• Used only when ablation is not feasible or declined.
• Rate control with beta-blockers or calcium channel blockers may be continued.
• Anti-arrhythmic therapy may be considered:
  • Amiodarone in structural heart disease or heart failure.
  • Flecainide or propafenone in patients without structural or ischaemic disease, but always with AV nodal blockade to prevent 1:1 conduction.

Anticoagulation

Initial anticoagulation

• If new-onset flutter and patient is not anticoagulated, start parenteral anticoagulation (unfractionated heparin or LMWH).
• Do not delay urgent cardioversion for anticoagulation if the patient is unstable.

Long-term anticoagulation

• Anticoagulation strategy mirrors that of atrial fibrillation.
• Use CHA₂DS₂-VASc to determine stroke risk.
• Assess bleeding risk with ORBIT or HAS-BLED.
• DOACs are first-line unless contraindicated.
• Warfarin remains appropriate for patients already stable on therapy.
• Anticoagulation is mandatory for at least 4 weeks post-cardioversion, even if sinus rhythm is restored.
• Long-term anticoagulation is recommended in recurrent flutter or when stroke risk is elevated.

Influence of underlying condition

• Prognosis is strongly determined by the presence of underlying cardiovascular or systemic disease.
• In around 60% of cases, atrial flutter develops during an acute medical process (e.g., infection, surgery, decompensated heart failure); once this is corrected, sinus rhythm is often restored and chronic therapy may not be necessary.
• Persistent or recurrent atrial flutter can precipitate tachycardia-induced cardiomyopathy, leading to repeated hospitalisations and progressive heart failure.

Risk of thromboembolism

• The risk of thromboembolic events in atrial flutter is similar to that of atrial fibrillation.
• Left atrial thrombus has been described in up to 21% of patients with atrial flutter who are not anticoagulated.
• Observational data suggest a 1.4-fold higher relative risk of stroke in patients with atrial flutter compared to controls.
• Concomitant atrial fibrillation further increases thromboembolic risk.
• Patients with Wolff–Parkinson–White syndrome and atrial flutter are at particular danger of 1:1 AV conduction and rapid ventricular response, potentially progressing to ventricular fibrillation.

Ventricular response and haemodynamics

• Compared with atrial fibrillation, atrial flutter often produces a faster ventricular rate due to fixed conduction ratios, making rate control more difficult.
• This contributes to haemodynamic compromise, with syncope and worsening heart failure being important clinical consequences.

Outcomes after ablation

• Catheter ablation for typical cavotricuspid isthmus–dependent flutter has an excellent prognosis, with recurrence rates below 5%.
• Ablation improves symptoms, prevents tachycardia-mediated cardiomyopathy, and reduces hospitalisation.
• The long-term outlook is more complex in patients with both atrial flutter and atrial fibrillation:
  • Some reports note reduced frequency of atrial fibrillation after flutter ablation.
  • Others show persistence of atrial fibrillation despite successful flutter ablation, though subsequent medical therapy may be more effective.

Complications of ablation procedures

• Large prospective series show low complication rates for ablation of typical flutter (<1%).
• Predictors of procedural complications include renal insufficiency and underlying structural heart disease.

Short-term outcomes in acute presentations

• A multicentre study of over 1000 emergency department patients with new-onset atrial fibrillation or flutter found:
  • Patients discharged in sinus rhythm had fewer adverse events within 30 days.
  • More than 10% experienced complications within this period, including stroke, though mortality was very low.
  • Risk factors for poor short-term outcomes included longer arrhythmia duration, pulmonary congestion on imaging, prior stroke/TIA, and discharge without rhythm restoration.

Prognostic modifiers

• Left atrial appendage thrombi are frequently observed in patients with new rapid atrial flutter and reduced ejection fraction, although their presence does not necessarily predict recovery of ventricular function.
• Patients with atrial flutter who are treated with class IC antiarrhythmic drugs may convert to flutter with rapid ventricular response; these patients must also be prescribed AV nodal blocking therapy to prevent dangerous conduction.

Thromboembolic events

• The most frequent and clinically important complication is embolic stroke, with reported left atrial thrombus rates ranging from 0–21% in patients with atrial flutter.
• The risk of systemic thromboembolism (stroke, peripheral embolism) approaches that seen in atrial fibrillation, particularly in the presence of comorbidities such as heart failure, hypertension, diabetes, or advanced age.
• Embolic risk is further heightened after left atrial ablation, as transseptal puncture and atrial scarring increase stroke potential.

Haemodynamic compromise

• Syncope, presyncope, or shock can develop in patients with poor haemodynamic reserve or during rapid ventricular conduction.
• Myocardial ischaemia may occur as demand exceeds supply, especially with poorly controlled ventricular rate.
• Acute pulmonary oedema and congestive heart failure are recognised complications, often requiring urgent intervention.

Tachycardia-mediated cardiomyopathy

• Prolonged rapid atrial flutter can lead to ventricular dysfunction and a reversible form of cardiomyopathy.
• This contributes to repeated hospitalisations with decompensated heart failure when flutter is uncontrolled.

Medication-related complications

Bradycardia

• May occur due to excessive AV nodal blockade with beta-blockers, calcium-channel blockers, or anti-arrhythmic drugs, especially in patients with intrinsic sinus node dysfunction.

Hypotension

• Vasodilatory effects of beta-blockers and calcium-channel blockers, combined with slowed conduction, may precipitate symptomatic hypotension.

Worsening heart failure

• Negative inotropic effects of nodal blockers and some anti-arrhythmics can exacerbate existing left ventricular dysfunction.

Proarrhythmia

• Class IC and Class III agents may precipitate ventricular tachycardia or torsade de pointes, particularly in those with structural heart disease or prolonged QT.
  
  

Thyroid dysfunction

• Amiodarone may cause both hypo- and hyperthyroidism due to its high iodine content.
• Routine thyroid monitoring is required; discontinuation may be necessary if thyroid dysfunction develops.

Pulmonary toxicity

• Long-term amiodarone use can cause pulmonary fibrosis, while acute administration may rarely cause acute respiratory distress syndrome.
• Pulmonary function monitoring every 6–12 months is advised during therapy.

Complications of ablation

• Right-sided ablation (cavotricuspid isthmus–dependent) carries a lower complication risk compared with left-sided ablation, which requires transseptal puncture.
• Reported risks include:
  • Pneumothorax (~0.2%).
  • AV fistula or vascular haematoma (<0.3%).
  • Pericardial effusion (up to 25%), tamponade (~1%).
  • Cerebrovascular events (0–4%).
  • AV block (<1%) or pacemaker requirement (<0.2%).
  • Organised atrial tachyarrhythmias after ablation (~13%).
• Procedure-related mortality is extremely rare (~0.03%).
• Most complications are manageable acutely, and overall ablation for typical flutter is considered highly safe.

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