📋 Key Information Summary
- AVNRT is the most common paroxysmal SVT — re-entry via dual AV nodal pathways; narrow-complex tachycardia ~150–250 bpm with pseudo-R′ in V1 and pseudo-S in inferior leads.
- AVRT (WPW syndrome) uses an accessory pathway — delta wave on resting ECG in pre-excitation; antidromic AVRT produces wide-complex tachycardia mimicking VT.
- Ventricular tachycardia (VT) originates below the His bundle; defined as ≥3 consecutive ventricular beats at rate ≥100 bpm; always assume VT in wide-complex tachycardia until proven otherwise.
- Haemodynamically unstable SVT/VT → synchronised DC cardioversion immediately (start at 120–150 J biphasic).
- Stable narrow-complex SVT → IV adenosine 6 mg rapid IV push → 12 mg → 12 mg as first-line diagnostic and therapeutic agent.
- Stable VT → IV amiodarone 300 mg over 20–60 min (or procainamide if structurally normal heart).
- ⚠️ AVNODAL blockers are CONTRAINDICATED in pre-excited AF (WPW + AF) — adenosine, verapamil, diltiazem, beta-blockers, digoxin can precipitate ventricular fibrillation and death.
- WPW + AF → procainamide IV or synchronised cardioversion; treat as VT-equivalent.
- ECG differentiation of SVT with aberrancy vs VT: favour VT if any of — capture beats, fusion beats, AV dissociation, extreme axis deviation, concordance in all precordial leads, QRS >160 ms.
- Catheter ablation is first-line long-term therapy for recurrent AVNRT, AVRT/WPW, and idiopathic VT with success rates >95% in Australian tertiary centres.
- Sustained monomorphic VT in structurally normal heart (RVOT, fascicular VT) — generally favourable prognosis; verapamil-sensitive fascicular VT responds to verapamil but NOT adenosine.
- Structural heart disease VT (ischaemic, dilated cardiomyopathy) — high risk of SCD; ICD indicated per NHFA/CSANZ guidelines if LVEF ≤35% despite ≥3 months optimal medical therapy.
- Pregnancy — adenosine remains first-line for haemodynamically stable SVT; avoid amiodarone (foetal thyroid toxicity); DC cardioversion safe in all trimesters.
- ATSI populations — higher prevalence of rheumatic heart disease predisposing to arrhythmias; reduced access to EP studies and ablation in remote communities; culturally safe pathways essential.
Introduction & Australian Epidemiology
Supraventricular tachycardias (SVTs) encompass a group of arrhythmias originating at or above the atrioventricular (AV) junction. Atrioventricular nodal re-entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT), including Wolff–Parkinson–White (WPW) syndrome, are the two most common paroxysmal SVTs encountered in Australian emergency departments and general practice. Ventricular tachycardia (VT) originates below the His bundle and carries a substantially higher risk of haemodynamic compromise, syncope, and sudden cardiac death (SCD).
In Australia, SVTs account for approximately 2–3 per 1,000 population, with AVNRT representing roughly 60% of paroxysmal SVTs and AVRT approximately 30%. VT incidence is estimated at 5–10 per 100,000 population per year, with the majority occurring in the context of structural heart disease — particularly ischaemic cardiomyopathy and dilated cardiomyopathy. Idiopathic VT in structurally normal hearts accounts for approximately 10% of all VT presentations.
Australian data from the AIHW National Hospital Morbidity Database indicate that arrhythmia-related admissions have increased by approximately 20% over the past decade, driven by improved detection (wearable monitors, implantable loop recorders) and an ageing population. The NHFA/CSANZ 2024 guidelines for the management of arrhythmias in Australia provide the framework for diagnosis and treatment discussed in this article.
Australian epidemiology snapshot: AVNRT has a female predominance (2:1 F:M) and typically presents in the 3rd–4th decade. AVRT/WPW has an equal sex distribution and manifests earlier (teens–20s). Structural-heart-disease VT is predominantly male (3:1) with median age >60 years.
AVNRT: Mechanism & ECG
Re-entrant Circuit
AVNRT is caused by re-entry within the AV node between two functionally distinct pathways:
- Slow pathway — inferior-posterior AV node input (compact node to coronary sinus ostium region); shorter refractory period, slow conduction velocity.
- Fast pathway — superior-anterior AV node input (compact node to Todaro tendon region); longer refractory period, fast conduction velocity.
Typical (Slow–Fast) AVNRT — ~90% of cases
Anterograde conduction via the slow pathway → retrograde conduction via the fast pathway. The P wave is buried within or immediately following the QRS complex (RP interval <70 ms). On ECG:
- Rate: 150–250 bpm (commonly 180–200 bpm).
- Narrow QRS complex (unless pre-existing bundle branch block or rate-related aberrancy).
- Pseudo-R′ wave in lead V1 (retrograde P distorting terminal QRS).
- Pseudo-S wave in leads II, III, aVF.
- No visible isoelectric segment between QRS and retrograde P.
Atypical (Fast–Slow) AVNRT — ~5–10%
Anterograde via fast pathway → retrograde via slow pathway. Produces a long RP tachycardia (RP interval > PR interval). P wave visible in early diastole — may be confused with atrial tachycardia or PJRT (permanent junctional reciprocating tachycardia).
Clinical pearl: AVNRT termination with adenosine or vagal manoeuvres (modified Valsalva in semi-recumbent position — 40 mmHg sustained for 15 s, then passive leg raise) confirms re-entrant SVT. Adenosine sensitivity is diagnostically valuable — if adenosine does not terminate the arrhythmia, consider atrial tachycardia or VT.
ECG Recognition Checklist
| Feature | Typical AVNRT | Atypical AVNRT |
|---|---|---|
| Circuit | Slow anterograde, fast retrograde | Fast anterograde, slow retrograde |
| RP interval | <70 ms (P buried/follows QRS) | >PR interval (long RP) |
| P-wave morphology | Pseudo-R′ V1; pseudo-S II/III/aVF | Negative P in II, III, aVF; positive in V1 |
| Prevalence | ~90% | ~5–10% |
| Adenosine response | Terminates | Terminates (may require higher dose) |
AVRT & WPW Syndrome
Anatomy of the Accessory Pathway
AVRT requires a structural accessory pathway (AP) — most commonly a free-wall or septal Kent bundle — providing a second conducting route between atria and ventricles separate from the AV node–His–Purkinje system. The AP may be:
- Manifest — conducts anterograde, producing pre-excitation (delta wave) on baseline ECG. The combination of a manifest AP + documented tachycardia = WPW syndrome.
- Concealed — conducts only retrograde; no delta wave at baseline; can still support orthodromic AVRT.
Orthodromic AVRT (~95% of AVRT)
Anterograde conduction via AV node → retrograde via AP. Produces a narrow-complex tachycardia with visible retrograde P wave (RP interval 70–90 ms, shorter than PR). The delta wave is absent during tachycardia because anterograde ventricular activation occurs through the normal conduction system.
Antidromic AVRT (~5%)
Anterograde via AP → retrograde via AV node. Produces a wide-complex tachycardia — maximally pre-excited QRS — which may be indistinguishable from VT on surface ECG. The rate is typically 200–300 bpm.
Pre-excitation ECG Features (Baseline)
- Short PR interval (<120 ms) — due to AV bypass conduction.
- Delta wave — slurred upstroke of QRS onset, widening the QRS to >110 ms.
- Secondary ST-T wave changes — discordant to the major QRS vector.
- Pathway localisation inferred from delta-wave polarity across precordial and limb leads (Arruda algorithm).
CRITICAL: Pre-excited atrial fibrillation (WPW + AF)
If a patient with WPW develops AF, conduction down the AP can produce ventricular rates exceeding 300 bpm with haemodynamic collapse → VF → cardiac arrest. AV nodal blockers are CONTRAINDICATED — adenosine, verapamil, diltiazem, beta-blockers, and digoxin all block the AV node, forcing all conduction through the AP and accelerating the ventricular response. Treatment: IV procainamide 15–18 mg/kg (max 50 mg/min) or synchronised DC cardioversion.
If a patient with WPW develops AF, conduction down the AP can produce ventricular rates exceeding 300 bpm with haemodynamic collapse → VF → cardiac arrest. AV nodal blockers are CONTRAINDICATED — adenosine, verapamil, diltiazem, beta-blockers, and digoxin all block the AV node, forcing all conduction through the AP and accelerating the ventricular response. Treatment: IV procainamide 15–18 mg/kg (max 50 mg/min) or synchronised DC cardioversion.
WPW + AF — ECG Recognition
- Irregularly irregular wide-complex tachycardia.
- Variable QRS morphology (fusion of AP and normal conduction).
- Very fast rate (often >220 bpm).
- Shortest pre-excited RR interval <250 ms = high risk of degeneration to VF.
Risk Stratification in WPW
Low Risk
Asymptomatic Pre-excitation
Incidental delta wave; no documented tachycardia; AP refractory period >250 ms on EP study; abrupt loss of pre-excitation with exercise testing or ajmaline challenge.
Setting: Outpatient EP referral for assessment
Moderate Risk
Symptomatic AVRT
Documented orthodromic AVRT; no AF; no haemodynamic compromise. Multiple pathways increase risk.
Setting: Elective EP study and catheter ablation
High Risk
WPW + AF or Syncope
Pre-excited AF; shortest pre-excited RR <250 ms; aborted SCD; multiple APs. AP effective refractory period <250 ms.
Setting: Urgent EP study + ablation; cardiology admission
Ventricular Tachycardia: Classification & ECG
Definition
Ventricular tachycardia is defined as ≥3 consecutive ventricular complexes at a rate ≥100 bpm. VT lasting <30 seconds that self-terminates is classified as non-sustained VT (NSVT); VT persisting ≥30 seconds or requiring intervention due to haemodynamic compromise is sustained VT.
Classification by Morphology
| Type | Morphology | Common Aetiology | Prognosis |
|---|---|---|---|
| Monomorphic VT | Constant QRS morphology beat-to-beat | Scar-related (ischaemic CM, DCM), RVOT-VT, fascicular VT | Variable — depends on structure |
| Polymorphic VT | Changing QRS axis/amplitude | Acute ischaemia, long QT, Brugada, catecholaminergic PMVT | High risk of degeneration to VF |
| Torsades de Pointes | Polymorphic VT with QTc prolongation | Drug-induced (sotalol, amiodarone, erythromycin), hypokalaemia, congenital LQTS | Self-terminating or degenerates to VF |
| Ventricular Fibrillation | Chaotic, no organised QRS | Ischaemia, electrical, commotio cordis | Immediate cardiac arrest |
Classification by Substrate
Structural Heart Disease VT (~90%)
- Post-myocardial infarction scar (re-entrant circuit around dense scar + border zone).
- Dilated cardiomyopathy (epicardial/mid-myocardial scar).
- Arrhythmogenic right ventricular cardiomyopathy (ARVC) — fat/fibro-fatty replacement of RV.
- Hypertrophic cardiomyopathy.
- Valvular heart disease, congenital heart disease post-repair.
Idiopathic / Structurally Normal Heart VT (~10%)
- RVOT VT — cAMP-mediated triggered activity; LBBB morphology, inferior axis; responds to adenosine, verapamil, beta-blockers.
- Fascicular VT (Belhassen VT) — re-entry within Purkinje network; RBBB + left axis (posterior fascicular); verapamil-sensitive.
- Outflow tract VT from LV — RBBB, inferior axis.
- LV summit / aortic cusp VT.
ECG Criteria: VT vs SVT with Aberrancy
In wide-complex tachycardia, assume VT until proven otherwise. Misdiagnosis of VT as SVT with aberrancy and treatment with AV nodal blockers can be fatal. The Brugada algorithm and Vereckei criteria provide systematic ECG differentiation:
| Criterion Favours VT | Sensitivity | Specificity |
|---|---|---|
| Absence of RS in all precordial leads (Brugada step 1) | 21% | 100% |
| RS interval >100 ms in any precordial lead (Brugada step 2) | 82% | 98% |
| AV dissociation (Brugada step 3) | 82% | 98% |
| Morphology criteria in V1/V6 (Brugada step 4) | 99% | 97% |
| Extreme axis deviation (northwest axis) | ~20% | ~95% |
| Concordance (all +ve or all −ve) across precordial leads | ~20% | ~95% |
| Capture beats / Fusion beats | ~5–10% | ~100% |
| QRS duration >160 ms (if LBBB pattern) or >140 ms (if RBBB pattern) | Variable | Variable |
When in doubt, treat as VT. The consequences of treating VT as SVT (AV nodal blocker → haemodynamic collapse) are far more dangerous than treating SVT with VT-directed therapy (amiodarone, cardioversion). If the patient is stable and diagnostic uncertainty persists, seek 12-lead ECG review, consider adenosine as a diagnostic trial (6 mg rapid push — if no response, do NOT give AV nodal blockers if any suspicion of VT or WPW).
Specific VT ECG Patterns
| VT Origin | ECG Pattern | Treatment Sensitivity |
|---|---|---|
| RVOT | LBBB + inferior axis (positive II, III, aVF) | Adenosine, verapamil, beta-blockers; ablation >90% |
| Posterior fascicular | RBBB + left axis deviation | Verapamil IV 5–10 mg; ablation >95% |
| Anterior fascicular | RBBB + right axis deviation | Verapamil; ablation |
| LV summit / aortic cusp | RBBB or LBBB; transition V1–V2 | Ablation from aortic root |
| Scar-related (ischaemic) | Variable; RBBB or LBBB; often monomorphic | Amiodarone; ICD; substrate ablation |
Acute Management
Universal First Step: Assess Haemodynamic Stability
At presentation, determine whether the patient is haemodynamically stable (conscious, talking, SBP >90 mmHg, no pulmonary oedema, no ongoing chest pain) or unstable (altered consciousness, hypotension, pulmonary oedema, ischaemic chest pain). This determines the immediate treatment pathway.
Haemodynamically unstable — any tachycardia (SVT or VT): Immediate synchronised DC cardioversion. Sedate if conscious (midazolam 1–2 mg IV or propofol 0.5–1 mg/kg). Biphasic energy: 120 J (SVT) or 200 J (VT/VF). Increase incrementally if unsuccessful.
Stable SVT (AVNRT / Orthodromic AVRT) — Acute Termination
1
Vagal Manoeuvres
Modified Valsalva: semi-recumbent position → blow into 10 mL syringe at 40 mmHg for 15 seconds → passive leg raise for 15 seconds. Success rate ~40% (vs ~17% for standard Valsalva). If unsuccessful, proceed to Step 2.
2
IV Adenosine
6 mg rapid IV push via large-bore cannula in antecubital fossa → flush with 20 mL NS immediately. If no response within 1–2 minutes: 12 mg IV rapid push → flush → repeat 12 mg if required. Success rate ~90–95%. Monitor ECG continuously — transient asystole (2–5 s) is expected. Adenosine 6 mg ampoule (Adenocor®) — ✔ PBS General Benefit.
3
IV Verapamil (if adenosine fails and narrow-complex SVT confirmed)
5 mg IV over 2 minutes → repeat 5–10 mg after 15–30 minutes if needed. Avoid in heart failure, wide-complex tachycardia, or suspected WPW. ✔ PBS General Benefit.
4
Synchronised DC Cardioversion
If pharmacological termination fails. Start at 120 J biphasic; escalate to 150–200 J. Sedate if conscious.
Pre-excited AF / Antidromic AVRT (WPW + AF)
DO NOT use adenosine, verapamil, diltiazem, beta-blockers, or digoxin. These block the AV node and force all conduction via the accessory pathway → ventricular rates >300 bpm → VF → death. Use: IV procainamide 15–18 mg/kg (max rate 50 mg/min) or synchronised DC cardioversion. Procainamide is available as Pronestyl® — ⚠ PBS Authority Required.
Stable VT — Acute Management
1
IV Amiodarone (Structural Heart Disease)
300 mg in 100 mL 5% dextrose IV over 20–60 min → maintenance 900 mg over 18–24 hours. Maximum cumulative dose 2.2 g in 24 h. Monitor for hypotension (rate-related), phlebitis. Amiodarone Cordarone® / generic — ✔ PBS General Benefit.
2
IV Procainamide (Structurally Normal Heart)
15–18 mg/kg IV over 30–60 min (max rate 50 mg/min). Effective for idiopathic VT and preferred over amiodarone when structurally normal heart confirmed. Monitor QTc; discontinue if QTc >500 ms or hypotension. ⚠ PBS Authority Required.
3
IV Verapamil (Fascicular VT ONLY)
5–10 mg IV over 2 min — ONLY if fascicular VT confirmed by ECG (RBBB + left axis, structurally normal heart). Do NOT use verapamil for VT of unknown aetiology — will cause haemodynamic collapse in structural heart disease VT.
4
Synchronised DC Cardioversion
If pharmacological therapy fails or patient deteriorates. 200 J biphasic. Ensure synchronisation mode selected. If degenerates to VF → unsynchronised defibrillation 200 J.
Torsades de Pointes — Specific Management
Torsades de Pointes: (1) Stop all QT-prolonging drugs immediately. (2) IV magnesium sulfate 2 g (8 mmol) in 100 mL NS over 5–10 min — even if serum magnesium is normal. (3) If recurrent or persistent: overdrive pacing (atrial or ventricular) at 90–110 bpm to shorten QT interval; or IV isoprenaline 1–4 mcg/min as bridge. (4) Correct hypokalaemia to K⁺ ≥4.5 mmol/L. (5) Avoid amiodarone and procainamide (further prolong QTc).
Long-term Treatment
AVNRT — Long-term Strategies
Catheter Ablation — Slow Pathway
First-line definitive therapy · Success >95% · Complication rate <1%
Procedure
Radiofrequency or cryoablation of slow AV nodal pathway. Performed via femoral venous access under local anaesthesia ± sedation.
Success rate
>95% acute success; recurrence <5% at 5 years
Major risk
Complete heart block requiring permanent pacemaker (~0.5–1%)
PBS status
✔ MBS Item 38286
Flecainide
Tambocor® · Class IC antiarrhythmic
Adult dose
50–100 mg PO BD (max 300 mg/day)
Paediatric dose
1–2 mg/kg/dose PO BD (max 8 mg/kg/day)
Route
Oral
Contraindication
Structural heart disease, ischaemic heart disease, LVEF <40% (CAST trial — increased mortality)
Renal adjustment
eGFR <35: reduce dose by 50%; monitor levels
PBS status
✔ PBS General Benefit
Sotalol
Sotacor® · Class III + beta-blocker
Adult dose
80–160 mg PO BD (initiate in hospital with 3-day monitored telemetry)
Paediatric dose
1–4 mg/kg/day PO divided BD (max 160 mg BD)
Renal adjustment
eGFR 30–60: 80 mg OD; eGFR 10–30: 80 mg every 24–48 h; eGFR <10: avoid
QTc monitoring
Discontinue if QTc >500 ms. Risk of Torsades de Pointes.
PBS status
✔ PBS General Benefit
AVRT / WPW — Long-term Strategies
- Catheter ablation of accessory pathway — first-line for all symptomatic WPW and for high-risk asymptomatic WPW (short AP refractory period, pre-excited AF). Success rate: left lateral pathways >97%, septal pathways 90–95%, right free-wall 88–93%. Risk of AV block for septal pathways (para-Hisian). MBS Item 38286.
- Pill-in-the-pocket (flecainide 200–300 mg single oral dose for self-terminating AVRT episodes) — only after in-hospital observation of first dose and ECG confirmation of safe termination. Not suitable for pre-excited AF.
- Medical therapy — if ablation declined or not feasible: flecainide (no structural heart disease) or sotalol. AV nodal blockers alone are insufficient as they do not block the AP.
VT — Long-term Strategies
Implantable Cardioverter-Defibrillator (ICD)
Indications per NHFA/CSANZ 2024:
- Secondary prevention — survivors of cardiac arrest due to VT/VF (without reversible cause), sustained VT with syncope or haemodynamic compromise, or VT with LVEF ≤35%. ICD is strongly recommended.
- Primary prevention — LVEF ≤35% despite ≥3 months of optimal guideline-directed medical therapy (GDMT) in ischaemic cardiomyopathy (post-MI ≥40 days) or non-ischaemic DCM. NYHA II–III. (MADIT-II, SCD-HeFT trials).
- Subcutaneous ICD (S-ICD) — preferred in younger patients, those requiring MRI, or with limited venous access. No anti-bradycardia pacing capability.
Amiodarone
Cordarone® / Aratac® · Class III
Loading
200 mg PO TDS × 1 week → 200 mg BD × 1 week → 200 mg OD maintenance
Maintenance
100–200 mg PO daily (aim for lowest effective dose)
Monitoring
TFTs (baseline, 3-monthly × 1 yr, then 6-monthly), LFTs, FBC, CXR, ophthalmology review annually
Key toxicity
Thyroid dysfunction (hypo > hyper), pulmonary fibrosis (1–5%), hepatotoxicity, corneal microdeposits, peripheral neuropathy, photosensitivity, blue-grey skin discolouration
Renal adjustment
None required (hepatically metabolised); active metabolite desethylamiodarone renally cleared — monitor in CKD
PBS status
✔ PBS General Benefit
Mexiletine
Mexitil® · Class IB · Adjunctive for refractory VT
Adult dose
200 mg PO TDS (max 1200 mg/day); start 200 mg BD and titrate
Role
Adjunct to amiodarone for refractory VT (ATMA trial); LQT3; Brugada syndrome
Side effects
GI (nausea, tremor); monitor levels (therapeutic 0.5–2.0 mg/L)
PBS status
⚠ PBS Authority Required
VT Ablation
- Idiopathic VT — curative (RVOT VT, fascicular VT): success >90%, low recurrence.
- Scar-related VT — substrate modification to reduce VT burden and ICD shocks. Success 50–70% freedom from VT at 1 year. Consider early referral if ≥1 appropriate ICD shock despite amiodarone, or recurrent VT episodes requiring hospitalisation.
- VT storm (≥3 VT episodes in 24 h) — IV amiodarone + sedation (propofol/midazolam) + catheter ablation or sympathetic denervation (left cardiac sympathetic denervation, stellate ganglion block).
Quick Reference: Long-term Therapy Selection
Recurrent AVNRT (no structural HD)
Catheter ablation (1st line); flecainide or sotalol if ablation declined
Avoid flecainide if LVEF <40%
WPW syndrome (symptomatic)
Catheter ablation of AP (1st line for all)
AV nodal blockers alone insufficient
RVOT VT / Fascicular VT
Catheter ablation (curative); beta-blockers or verapamil as medical Rx
Fascicular VT → verapamil-sensitive
VT in ischaemic CM (LVEF ≤35%)
ICD + GDMT + amiodarone; VT ablation if recurrent
Optimise HF therapy ≥3/12 before ICD
VT storm
IV amiodarone + sedation + ablation; consider sympathetic denervation
ICU / cardiac catheterisation lab
Special Populations
Pregnancy
SVT in pregnancy
First-line: vagal manoeuvres → adenosine 6 mg IV rapid push (safe in all trimesters, ultra-short half-life). DC cardioversion safe at any gestation. Avoid verapamil (limited safety data). Beta-blockers (metoprolol, labetalol) can be used if needed.
VT in pregnancy
DC cardioversion is safe. Avoid amiodarone — causes foetal hypothyroidism, goitre, growth restriction. If antiarrhythmic needed: procainamide or flecainide (limited data, but preferred over amiodarone). Peripartum cardiomyopathy VT: amiodarone may be necessary if life-threatening — discuss with obstetric/cardiology MDT.
Catheter ablation
Generally deferred to post-partum unless life-threatening arrhythmia. Fluoroscopy should be minimised; zero-fluoroscopy ablation (electroanatomical mapping) techniques increasingly available in Australian centres.
Paediatrics
Neonatal SVT
Often presents as irritability, poor feeding, tachycardia >220 bpm. IV adenosine 0.1 mg/kg (max 6 mg) rapid push. If refractory: IV amiodarone 5 mg/kg over 20–60 min or synchronised cardioversion 0.5–1 J/kg biphasic. Many neonatal accessory pathways undergo spontaneous involution by age 1 year.
Childhood SVT
Adenosine 0.1 mg/kg (max 6 mg) → 0.2 mg/kg (max 12 mg). Vagal manoeuvres: ice-water-soaked towel on face (infants), Valsalva (older children). Prophylaxis: flecainide 1–2 mg/kg/dose BD (no structural HD) or sotalol 1–4 mg/kg/day divided BD. Catheter ablation generally deferred until ≥15 kg / age ≥5 years unless refractory.
Paediatric VT
Uncommon. Consider: post-surgical congenital HD, channelopathies (CPVT, LQTS), myocarditis. Anti-tachycardia pacing for ICD recipients. Amiodarone 5 mg/kg load; procainamide 15 mg/kg (older children).
Elderly
Age-related considerations
Higher prevalence of structural HD, AF + SVT overlap, renal impairment affecting drug clearance. Adenosine may be less effective at terminating AVNRT in elderly (faster AV nodal conduction); may require higher doses. Rate-limiting agents: use with caution due to hypotension risk. Catheter ablation success rates are equivalent but procedural risks slightly higher.
ICD in elderly
Shared decision-making required. Consider frailty, life expectancy, comorbidities, patient goals. NHFA/CSANZ: ICD benefit diminishes if estimated survival <1 year from non-cardiac causes.
Renal Impairment
Drug adjustments
Adenosine: no adjustment (half-life 10 seconds). Sotalol: dose reduce per eGFR (renally cleared — see dosing table above). Flecainide: reduce dose if eGFR <35 mL/min. Amiodarone: no dose adjustment but active metabolite accumulates — monitor QTc closely. Digoxin: reduce dose and monitor levels (target 0.5–0.9 ng/mL in arrhythmia).
Dialysis patients
Electrolyte shifts during haemodialysis may trigger arrhythmias. Avoid sotalol (accumulates). Amiodarone preferred. Haemofiltration does not significantly clear amiodarone.
Hepatic Impairment
Drug considerations
Amiodarone: hepatically metabolised — significant accumulation risk in severe hepatic impairment (Child–Pugh B/C); avoid if possible. Flecainide: hepatically metabolised — reduce dose in hepatic impairment. Sotalol: renally cleared — no hepatic adjustment required. Adenosine: no hepatic adjustment.
Immunocompromised
Drug interactions
Amiodarone is a potent CYP3A4 and P-glycoprotein inhibitor — interacts with tacrolimus, cyclosporine, sirolimus (immunosuppressant levels increase). Monitor drug levels closely. QT-prolonging interactions with azole antifungals (fluconazole, voriconazole) and macrolides (azithromycin) — additive risk of Torsades. Oncology patients on anthracyclines — increased cardiotoxicity risk with amiodarone.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
📚 References
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