2.3 Cardiac Arrhythmias & Syncope

Cardiac Arrhythmias & Syncope

Cardiac arrhythmias represent a frequent cause of acute hospital presentations, palpitations, lightheadedness, and sudden cardiac death. The Resuscitation Council UK (RCUK) and NICE guidelines establish a rapid, unified clinical approach based on haemodynamic stability, QRS complex duration, and rhythm regularity.

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1. The Emergency Approach: Adverse Clinical Features

Whenever a patient presents with an acute tachyarrhythmia or bradyarrhythmia, the initial priority is to determine whether life-threatening adverse features are present (the "Rule of 4"):

1. Shock: Hypotension (systolic blood pressure <90 mmHg), pallor, diaphoresis, cold clammy extremities, confusion, or impaired consciousness.
2. Syncope: Transient loss of consciousness resulting from global cerebral hypoperfusion.
3. Myocardial Ischaemia: Typical anginal chest discomfort or diagnostic ischaemic ECG changes (ST depression or elevation).
4. Severe Heart Failure: Pulmonary oedema (bilateral lung crackles, respiratory distress) or elevated jugular venous pressure.

The Golden Resuscitation Rule

• If ANY adverse feature is present in TACHYCARDIA: Perform immediate emergency synchronised DC cardioversion (up to 3 shocks, 120–150 J biphasic escalating) under conscious sedation or intravenous anaesthesia. Synchronisation ensures the electrical shock is delivered on the R wave, preventing discharge during the vulnerable T-wave repolarisation phase which would induce ventricular fibrillation (the "R-on-T" phenomenon).
• If ANY adverse feature is present in BRADYCARDIA: Administer intravenous Atropine 500 mcg bolus, repeated every 3–5 minutes to a maximum of 3 mg, and prepare immediate transcutaneous cardiac pacing.

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2. Atrial Fibrillation (AF)

Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting over 1.5 million people in the United Kingdom and conferring a five-fold increase in the risk of ischaemic stroke.

Electrocardiographic Features

• Completely absent P waves.
• An irregular, undulating baseline consisting of low-amplitude fibrillatory waves (f-waves) at 300–600 cycles/min.
• An irregularly irregular ventricular response (variable R-R intervals).
• Narrow QRS complexes (<120 ms), unless pre-existing bundle branch block or rate-dependent aberrancy coexists.

Rate Control vs. Rhythm Control

In haemodynamically stable patients without adverse features, clinicians must choose between rate control and rhythm control strategies:

• Rate Control (Standard First-Line):
  • Recommended for the majority of patients, particularly those aged >65 years, with coronary disease, or with asymptomatic/mildly symptomatic persistent AF.
  • First-line monotherapy: A cardioselective beta-blocker (e.g. Bisoprolol 2.5–10 mg once daily) OR a rate-limiting non-dihydropyridine calcium channel blocker (e.g. Verapamil 40–120 mg TDS or Diltiazem 60–120 mg TDS).
  • Digoxin Monotherapy: Reserved strictly for sedentary, non-ambulatory elderly patients, particularly those with concomitant heart failure. Digoxin acts via parasympathomimetic AV-nodal inhibition; it successfully controls resting heart rate but fails during exertion or high sympathetic tone.
  • Treatment Target: Initial resting heart rate <110 bpm (lenient rate control) is acceptable if asymptomatic; target <80 bpm if symptoms persist or left ventricular dysfunction develops.
• Rhythm Control:
  • Indicated if: (1) patient remains symptomatic despite optimal rate control; (2) younger active patients; (3) first presentation of acute-onset AF (<48 hours); (4) heart failure clearly precipitated by AF (tachycardiomyopathy); or (5) secondary to an acute reversible precipitant (e.g. pneumonia, hyperthyroidism, pulmonary embolism).
  • Pharmacological Cardioversion: Flecainide (class 1c; IV 2 mg/kg over 10–30 minutes, maximum 150 mg, or a single oral dose of 200–300 mg) in patients with structurally normal hearts (strictly contraindicated in ischaemic or structural heart disease due to proarrhythmic risk). Alternatively, IV Amiodarone (300 mg infused over 20–60 minutes, followed by 900 mg over 24 hours) is preferred if structural heart disease or heart failure is present.
  • Electrical Cardioversion: Elective synchronised DC cardioversion.
  • The 48-Hour Anticoagulation Rule: If AF duration exceeds 48 hours (or the onset is uncertain), cardioversion carries high risk of dislodging an organised left atrial appendage thrombus. Cardioversion must be delayed until the patient has received at least 3 consecutive weeks of therapeutic anticoagulation, or until a transoesophageal echocardiogram (TOE) conclusively rules out left atrial thrombus. Therapeutic anticoagulation must be continued for at least 4 weeks post-cardioversion in all patients.

Stroke Risk: The CHA2DS2-VASc Score

All non-valvular AF patients must be risk-stratified for systemic thromboembolism using the validated CHA2DS2-VASc tool:

• Anticoagulation Recommendations (NICE):
  • Score ≥2 (men or women): Offer anticoagulation with a DOAC (NICE NG196).
  • Score 1 in men: Consider anticoagulation with a DOAC, taking bleeding risk into account.
  • Score 0 in men or 1 in women (sex as the only risk factor), aged under 65: Do not offer stroke prevention therapy.
  • First-Line Choice: Direct Oral Anticoagulants (DOACs)—Apixaban (5 mg BD), Rivaroxaban (20 mg OD), Edoxaban (60 mg OD), or Dabigatran (150 mg BD)—are preferred over Warfarin due to superior safety, lower intracranial bleeding rates, fixed dosing, and no requirement for routine INR monitoring.
  • Warfarin (target INR 2.0–3.0) is used when a DOAC is contraindicated, not tolerated or unsuitable, and is the anticoagulant for mechanical prosthetic heart valves or moderate-to-severe mitral stenosis ("valvular AF"), where DOACs are not used.

Bleeding Risk: ORBIT (NICE) and HAS-BLED

Since 2021, NICE NG196 recommends the ORBIT score because it predicts absolute bleeding risk more accurately than other tools: Older age (75 or over, 1 point), Reduced haemoglobin or haematocrit or a history of anaemia (2 points), Bleeding history (2 points), Insufficient kidney function (eGFR below 60, 1 point) and Treatment with an antiplatelet (1 point); 0–2 is low, 3 medium and 4–7 high risk. HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding, Labile INR, Elderly over 65, Drugs/alcohol) is the older tool still used in ESC guidance and many hospitals. A high bleeding score is not on its own a reason to withhold anticoagulation; it prompts correction of modifiable risk factors (controlling blood pressure, stopping NSAIDs or unnecessary antiplatelets, reducing alcohol) and closer review.

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3. Tachycardia Diagnostic Algorithm

In haemodynamically stable patients, rhythm classification relies on two ECG features: QRS duration (<120 ms vs. ≥120 ms) and rhythm regularity (regular vs. irregular).

A. Regular Narrow-Complex Tachycardia (QRS <120 ms)

Most commonly Supraventricular Tachycardia (SVT), including Atrioventricular Nodal Re-entrant Tachycardia (AVNRT; 60%) and Atrioventricular Re-entrant Tachycardia (AVRT; 30%, involving an accessory pathway as in Wolff-Parkinson-White syndrome):

1. Step 1: Vagal Manoeuvres: Increase parasympathetic outflow to the AV node. The modified Valsalva manoeuvre (forced expiration against a 40 mmHg manometer for 15 seconds while seated, followed immediately by passive supine positioning with 45° leg elevation for 15 seconds) converts over 40% of SVTs. Carotid sinus massage (auscultate for bruits first; avoid if prior TIA/stroke) is an alternative.
2. Step 2: Intravenous Adenosine:
   • If vagal manoeuvres fail, administer Adenosine 6 mg as a rapid intravenous push via a large-bore cannula in the antecubital fossa, immediately followed by a rapid 20 mL 0.9% saline flush.
   • If unsuccessful after 1–2 minutes, administer Adenosine 12 mg rapid IV bolus.
   • If still unsuccessful after another 1–2 minutes, administer a final bolus of Adenosine 18 mg rapid IV.
   • Mechanism: Activates A1 purinergic receptors in the AV node, driving hyperpolarisation and transient complete AV conduction block. Warn the patient of transient sensations of intense flushing, dyspnoea, chest pressure, and impending doom.
   • Contraindications: Severe active asthma or bronchospasm (can trigger severe bronchospasm), severe second/third-degree heart block, or decompensated heart failure. Alternative agent: IV Verapamil 2.5–5 mg over 2 minutes.

B. Irregular Narrow-Complex Tachycardia

Almost always Atrial Fibrillation, Atrial Flutter with variable block, or multifocal atrial tachycardia (MAT, commonly seen in severe COPD). Treat as AF with rate control.

C. Regular Broad-Complex Tachycardia (QRS ≥120 ms)

• Universal Rule: Treat any broad-complex regular tachycardia as Ventricular Tachycardia (VT) until proven otherwise (>80% of cases). Never give adenosine or verapamil blindly to an undifferentiated broad-complex tachycardia, as this can precipitate cardiovascular collapse if VT is present.
• Treatment in Stable VT: Intravenous Amiodarone 300 mg infused over 20–60 minutes, followed by an intravenous infusion of 900 mg over the subsequent 24 hours. If drug therapy fails or deterioration occurs, perform synchronised DC cardioversion.
• Polymorphic VT (Torsades de Pointes): Characterised by continuously twisting QRS complexes around the isoelectric line, typically triggered by prolonged QT interval (e.g. hypokalaemia, hypomagnesaemia, macrolides, psychotropics). Treatment: Intravenous Magnesium Sulphate 2 g over 10 minutes, correction of electrolytes, and withdrawal of QT-prolonging drugs.

D. Irregular Broad-Complex Tachycardia

Differentials include AF with pre-existing bundle branch block, polymorphic VT, or Pre-excited AF (AF with Wolff-Parkinson-White syndrome). In pre-excited AF, conduction occurs down an accessory bypass tract (Bundle of Kent), producing an irregular, bizarre, very wide QRS rhythm. Contraindication: AV-nodal blocking drugs (adenosine, verapamil, beta-blockers, digoxin) are strictly contraindicated because blocking the AV node shunts all impulses down the accessory pathway, precipitating ventricular fibrillation. Treatment: seek expert help; synchronised DC cardioversion is the safest option (urgent if unstable), and any drug treatment is a specialist decision.

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4. Bradyarrhythmias & Conduction Blocks

Bradycardia (heart rate <60 bpm) may be physiological (athletes, sleep) or pathological:

Atrioventricular (AV) Blocks

• First-Degree AV Block: Constant, prolonged PR interval >200 ms (>5 small squares). Every P wave conducts to a QRS complex. Benign; no treatment required.
• Second-Degree AV Block Mobitz Type I (Wenckebach): Progressive lengthening of the PR interval until a P wave fails to conduct (dropped QRS). The cycle then repeats. Conduction defect is within the AV node itself. Usually benign, often vagally mediated or inferior ischaemia; treat only if symptomatic.
• Second-Degree AV Block Mobitz Type II: Constant, unchanging PR intervals with intermittently non-conducted P waves (e.g. 2:1, 3:1 block). The defect is in the infranodal His-Purkinje system. High risk of sudden progression to complete heart block and asystole. Requires urgent hospital admission, cardiac telemetry, transcutaneous pacing pads, and a permanent pacemaker (PPM).
• Third-Degree (Complete) Heart Block: Complete failure of AV conduction. P waves and QRS complexes beat entirely independently (AV dissociation). Atrial rate (~60–80 bpm) exceeds the slow ventricular escape rate (~30–45 bpm). High risk of syncope (Stokes-Adams attacks) and sudden death. Requires urgent admission, transcutaneous pacing on standby, and permanent pacemaker implantation.

Acute Bradycardia Management Protocol

1. Assess for adverse features: shock, syncope, myocardial ischaemia, or acute heart failure.
2. If adverse features present: Administer Atropine 500 mcg IV. Repeat every 3–5 minutes up to a maximum of 3 mg.
3. If atropine fails or risk of asystole is high (recent asystole, Mobitz II, complete heart block with wide QRS, ventricular pause >3 seconds): Initiate transcutaneous pacing immediately, or start an intravenous infusion of Isoprenaline (5 mcg/min) or Adrenaline (2–10 mcg/min). Arrange urgent transvenous temporary pacing wire insertion.

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5. Syncope: Assessment & Red Flags

Syncope is defined as a transient loss of consciousness (TLOC) caused by transient global cerebral hypoperfusion, characterised by rapid onset, brief duration, and spontaneous complete recovery without neurological deficit.