Tag: af

Atrial Fibrillation/Flutter

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It’s essential any Modifiable causes are treated, these include:

    • Haemodynamic stress: Valvular disease/Hypertension/LVD/Thrombus
    • Atrial ischemia: Ischaemic Heart Disease
    • Inflammation: Sepsis/Myocarditis/pericarditis
    • Noncardiovascular respiratory causes: PE/Pneumonia/Lung Cancer
    • Alcohol and drug use: Alcohol/Cocaine/Amphetamine
    • Endocrine disorders: Hyperthyroid/Diabetes/Phaeochromacytoma/Electrolyte prob.
    • Neurologic disorders: Subarachnoid Haemorrhage/Stroke
    • Genetic factors
    • Advancing age

Tests (NEW AF)

  • 12 Lead ECG
  • Bloods: FBC, U&E, Bone profile, Magnesium, LFT, TFT, Clotting, Glucose
  • Others: individualised to the patient.
  • First line:
    • β-Blocker – outperforms calcium channel blockers in studies
    • Non-dihydropyridine calcium channel blockers (Diltiazem/Verapamil) – esp. in Severe COPD/Asthma
  • Second Line:Consider adding in
    • Digoxin – however, digoxin alone is not effective in patients with increased sympathetic drive. Observational studies have associated digoxin use with excess mortality in AF patients)
    • Amiodarone can be useful as a last resort when heart rate cannot be controlled with combination therapy in patients who do not qualify for non-pharmacological rate control

Rhythm control in ED

“Early cardioversion is not recommended without appropriate anticoagulation or transoesophageal echocardiography if AF duration is longer than 24 h, or there is scope to wait for spontaneous cardioversion.”

In reality risks increase beyond 12hrs from onset, and those reverted in ED will often return to AF by the time they get to AF clinic follow up.

AF increases the chance of Stroke by 5x (and those recently diagnosed are least likely be on any form of protection)

  • ESC/NICE recommends using the CHADS-VASc to assess stroke risk and ORBIT to assess bleeding risk
  • There are currently significant delays getting to “New AF” clinic as well as to GP’s, making assessment of Stroke risk in ED more important than ever

CHADS-VASc outcome recommendations

    • Males (0), Female (1) – No anticoagulation recommended
    • Males (1) – Consider anticoagulation (DOAC) in light of bleed risk
    • ALL (≥2) – Anticoagulation recommended (DOAC)- Trust DOAC guide,  NICE/CKS
    • Use Apixaban where first line, significantly cheaper. If using alternative please document reasons.

ORBIT outcome recommendations

    • Modifiable risks – Address ALL modifiable risk factors
    • Most will benefit from anticoagulation – but discuss personalised risk with patients

Contraindications to Anticoagulation inc:

    • Active serious bleeding (where the source should be identified and treated)
    • Associated comorbidities (e.g. severe thrombocytopenia <50 platelets/lL, severe anaemia under investigation, etc.)
    • Recent high-risk bleeding event such as intracranial haemorrhage (ICH).
  • Life Style
    • Obesity: Risk of AF, Recurrence of AF and Stoke all increase with BMI
    • Alcohol: Alcohol excess both increases the risk of AF and of Bleeding, so patient should support to reduce aldol intake is recommended
    • Caffeine: It is unlikely caffeine consumption causes AF. Habitual caffeine use may reduce the risk of developing AF. But increases the symptoms
    • Exercise: Moderate cardiavasclar exercise is protective, however higher rates of AF are seen in elite athletes and vigorous physical activity
  • Specific conditions- patient should follow up with GP/Clinic (treatment may start in ED)
    • Hypertension
    • Heart Failure
    • Coronary artery disease
    • Diabetes Mellitus
    • Sleep Apnoea

Arrhythmia clinic is for patients with newly diagnosed and symptomatic AF/SVT (if the patient is not symptomatic they should be followed up through their GP).

It should be remembered that patients will be seen after at least 6 weeks so anticoagulation decisions should not be delayed for clinic.

GUIDANCE

Based primarily on:

EMbeds clinical quick guide

Last evidence review: October 2026
Suggested next review: October 2026

This is a clinical support guide and does not replace clinical judgement, current CHFT medicines guidance or specialist advice.

Tachycardia

Adult ED Management – RCUK 2025

Treat the patient, not the rate

Sinus tachycardia is usually compensatory — identify and treat the cause. Do NOT cardiovert sinus tachycardia.

INITIAL ASSESSMENT

ABCDE

Cardiac monitor
BP and SpO₂
12-lead ECG
IV access
Bloods as clinically indicated: FBC
U&E / Mg²⁺ / Ca²⁺
glucose
troponin where indicated
other investigations directed by likely cause
Give oxygen only if SpO₂ <94%, unless an alternative target is appropriate.

Think WHY the patient is tachycardic?

Sepsis/Hypovolaemia/Haemorrhage
Pain/Anxiety
Hypoxia
Fever
PE
ACS/Heart failure
Thyrotoxicosis
Drugs/Withdrawal
Pregnancy

Do not attempt to normalise an appropriate sinus tachycardia with anti-arrhythmics or electrical cardioversion.

SIMPLE ED RULE

SICK? → SHOCK

WELL? → WIDTH + REGULARITY

  • Narrow + regular: Vagal → Adenosine → Verapamil / beta-blocker → Shock
  • Narrow + irregular: AF pathway / rate control
  • Broad + regular: VT until proven otherwise → Cardioversion / procainamide
  • Broad + irregular: Pre-excited AF / polymorphic VT → expert help

UNSTABLE?

LIFE-THREATENING FEATURES

> SHOCK: Hypotension with evidence of impaired tissue perfusion.
> SYNCOPE: Especially with severe or ongoing hypotension.
> MYOCARDIAL ISCHAEMIA: Ongoing chest pain and/or significant ischaemic ECG changes.
> SEVERE HEART FAILURE: Particularly pulmonary oedema.
> IMMEDIATELY POST-ROSC

DC-Cardiversion (SYNC) RCUK 2025

> AF → Maximum defibrillator output
> Flutter / SVT → 70–120 J
> VT with pulse → 120–150 J

Escalate subsequent shocks where appropriate.

STABLE

Regular  – Sinus Tachycardia, AVNRT (SVT), Atrial flutter with regular block, AVRT (WPW)

  • Sinus Tachycardia – Look for the cause ?infection ?pain ?anaemia ?hypovolaemia ?anxiety ?drugs
  • SVT – Stepwise treatment until NSR regained (ensure cardiac monitoring): –
    • Vagal Manoeuvres – Lie flat and head down, Carotid sinus massage (ensure no bruit 1st), Blow into 50ml syringe
    • Adenosine –  6mg, 12mg, 18mg boluses (not in severe Asthma/Allergy/Heart transplant)
    • Not reverted – call for expert help
  • Atrial Flutter with 2:1 block (150bpm) – consider rate controlling drugs
  • AVRT (WPW) – get expert help (DO NOT give Adenosine)

PDF: Arrhythmia Clinic referral form (Print and Fax OR can email – use fill and sign function to enter details)

PDF: Patient Info

Irregular – likely AF (Follow AF Pathway)

Assume VT until proven otherwise

Particularly in:

  • older patients
  • previous MI
  • structural heart disease
  • cardiomyopathy

Stable monomorphic VT

Electrical cardioversion is an appropriate first-line strategy

  • Especially where structural heart disease is present or cannot be excluded.
  • SYNCHRONISED CARDIOVERSION For VT with a pulse: 120–150 J initially, escalating if required

If sedation / anaesthesia presents significant risk

Drug treatment may be considered:

  • Procainamide 10–15 mg/kg IV over 20 minutes Maximum 1 g OR
  • Amiodarone 300 mg IV over 10–60 minutes followed by: 900 mg IV over 24 hours
  • If ineffective: SYNCHRONISED CARDIOVERSION WITH EXPERT ADVICE

STOP — HIGH-RISK RHYTHM

Consider:

  • 1. AF WITH BUNDLE BRANCH BLOCK
  • 2. PRE-EXCITED AF / WPW
  • 3. POLYMORPHIC VT

Seek senior / cardiology support early.

PRE-EXCITED AF

Think pre-excitation when there is:

  • very rapid irregular broad-complex tachycardia
  • varying QRS morphology
  • ventricular rates sometimes >200 bpm
  • known WPW / previous delta wave

DO NOT GIVE AV-NODAL BLOCKING DRUGS

Avoid the following as these may increase conduction through the accessory pathway and precipitate VF:

  • Adenosine
  • Beta-blockers
  • Verapamil
  • Diltiazem
  • Digoxin

Treatment

  • Procainamide OR
  • Synchronised cardioversion

If polymorphic VT occurs with QT prolongation:

Magnesium: Mg²⁺ 8 mmol IV over 10 minutes

Also:

  • Correct K⁺ / Mg²⁺ abnormalities.
  • Stop QT-prolonging drugs.
  • Treat reversible causes.
  • Seek expert help.

For recurrent pause-dependent torsades consider increasing the heart rate with:

  • Isoprenaline OR
  • Temporary pacing

❌ AVOID AMIODARONE because it may further prolong the QT interval.

⚠️ PITFALLS

FAST ≠ ARRHYTHMIA

Do not treat physiological sinus tachycardia as an arrhythmia.

BROAD + REGULAR = VT UNTIL PROVEN OTHERWISE

Do not delay appropriate treatment while attempting to prove SVT.

BROAD + IRREGULAR ≠ ROUTINE AF

Always consider pre-excited AF.

ADENOSINE IS NOT FOR IRREGULAR BROAD-COMPLEX TACHYCARDIA

DO NOT GIVE AMIODARONE FOR TORSADES / LONG-QT POLYMORPHIC VT

Give magnesium and correct the underlying problem.

CARDIOVERSION REQUIRES SYNC

Confirm the machine is marking the R waves before delivering the shock.

Re-check SYNC after each shock — some defibrillators automatically revert out of synchronised mode.

DISPOSITION

Consider admission / cardiology assessment for:

  • VT
  • broad-complex tachycardia of uncertain cause
  • syncope associated with tachyarrhythmia
  • significant structural heart disease
  • ACS / myocardial ischaemia
  • heart failure
  • recurrent arrhythmia despite treatment
  • pre-excitation
  • significant electrolyte disturbance
  • drug-induced arrhythmia
  • prolonged QT / torsades
  • haemodynamic instability
  • arrhythmia requiring electrical cardioversion

Patients with uncomplicated successfully terminated SVT may be suitable for discharge following senior review, appropriate investigation and follow-up depending on the clinical circumstances.

GUIDANCE

Based primarily on:

  • Resuscitation Council UK — Guidelines 2025: Adult Advanced Life Support
  • Resuscitation Council UK — Adult Tachyarrhythmia Algorithm, current version March 2026
  • Current atrial fibrillation guidance

EMbeds clinical quick guide

Last evidence review: September 2026
Suggested next review: September 2027

This is a clinical support guide and does not replace clinical judgement, current CHFT medicines guidance or specialist advice.