Arrhythmias

Definition:

  1. Deviation from regular sinus rhythm of 60–100bpm. May be one or more of: irregular, faster (tachyarrhythmias), slower (bradyarrhythmias), or not generated from SA node (ectopic).

Conduction system

  1. SA Node:
    1. Junction of RA & SVC. Linked to AV node by atrial internodal pathways
    2. Supplied by RCA in 55–60%, otherwise L circumflex
    3. Innervated by symp & parasymp.
    4. Native discharge rate is 90–100bpm (↓ by parasymp tone to ~70–80bpm)
  2. AV Node
    1. RA myocardium nr septal leaflet of TV in otherwise non-conducting annular fibrosis
    2. Supplied by RCA in 90%, 10% by LC circumflex
    3. Slower conduction 0.05m/s to allow for atrial contraction
  3. Remainder of conduction system
    1. Bundle of His runs in membranous septum
    2. Splits into right & left bundles. The latter splits into ant. & post. Fascicles.
    3. Right bundle & L ant. Fascicle supplied by AV nodal art. in 50% & LAD in rest.
    4. Left post. fasc supplied by AV nodal only in 50% & by both AV nodal & LAD in rest.
    5. Bundles/fascicles are composed of fast conducting Purkinje fibres.
    6. Embryonic myocardium remnants around the AV node can → accessory pathways.

Arrhythmia Mechanisms

  1. Tachyarrhythmias
    1. Re-entry circuits – unidirectional, can be micro (AF, VF) or macro (PSVT)
    2. Enhanced automaticity – ectopic foci
    3. After polarizations – oscillations of mem pot → another depolarization. E.g. TdP
    4. Bradyarrhythmias
      1. Depression of SA node
      2. Conduction system block

Causes

  1. IHD – most common of serious acute arrhythmias
  2. CHD – valvular, myocardial defects, HOCM, prolonged QT syndromes
  3. Structural – cardiomyopathies, acq. Valve defects, HT
  4. Electrolyte disturbance – high or low K , low Mg2 or Ca2
  5. Metabolic – hypoxia, hypercarbia, acidosis, hypothermia, hyperthyroidism, phaeo.
  6. Drugs – antiarrhythmics, cocaine, amphetamines, TCA, Na or K channel blockers
  7. Trauma – commotio cordis – VF from blunt chest trauma.

Principles of management

  1. Triaged to an area where they can be monitored and sequelae of arrhythmia managed.
  2. Resuscitate/ABCs – ?arrest, shock, APO, ↓GCS. If unstable, cardioversion/pacing likely.
  3. IVC bloods for UEC, CMP, FBC ± cardiac biomarkers ± TFTs ± drug levels (e.g. digoxin)
  4. ECG (classify & diagnose arrhythmia) ± CXR
  5. Rx aimed at restoring adequate cerebral perfusion, a reg. rhythm & treat precip conds.

Management Options

  1. No Rx:
    1. If no resus required.
    2. May be approp: sinus arrhythmia, atrial ectopics, non R-on-T ventricular ectopics, accel idioventricular rhythm, AF in assoc with hypothermia, Mobitz type I 2° block.
  2. Non-Pharmacological
    1. Vagal manoeuvres – Valsalva, carotid sinus massage, diving reflex. Avoid ocular massage, PR.
    2. Precordial thump – immediate response to monitored VF/pulseless VT
  3. Pharmacological
    1. Electrolyte correction
    2. Usual first line if haemodynamically stable and arrhythmia needs treatment.
  4. Electrical
    1. Cardioversion
      1. Haemodynamically unstable or drug-resistant tachyarrhythmias.
    2. Pacing
      1. Transcutaneous, transvenous, overdrive
      2. Drug-resistant brady & tachyarrhythmias.

Vaughan-Williams Classification of antiarrhythmics – limited usefulness

  1. Class I (Fast Na channel blockers)
    1. Class Ia (slow conduction, ↑QRS & ↑QT)
      1. Procainamide: IV 17mg/kg (12mg/kg if APO) load then 2.8mg/kg/hr (halve if APO). SE: ↓BP, ↓HR, lupus-like syndrome
      2. Disopyramide: PO. Slow Abs. 1/3 Metab liver. Renal excr. Neg. ionotrope.
      3. Quinidine: Rare in Aus. 200–400mg q2h PO to max 1g or 600–800mg PO stat. SE: cinchonism (tinnitus, vis.dist., headache, vertigo, confusion)
    2. Class Ib (prolong refractory period)
      • Lignocaine: 1.5mg/kg bol. max 3mg/kg. Maint 2mg/min IV. SE: ↓BP,CNS tox
      • Phenytoin
    3. Class Ic (depress conductivity, ↑QRS, ↑PR, ↑AV block)
      • Flecainide: 2mg/kg over 20min. SE: proarrhythmic in structural/IHD
  2. Class II (β-blockers) e.g. atenolol, metoprolol, esmolol, sotalol
  3. Class III (prolong repol. by K efflux, ↑QRS, ↑PR & ↑QT)
    1. Sotalol: 0.5–1.5mg/kg IV/PO. CI: COAD, DM, PVD, LVF, hypoK , bradycardic
    2. Amiodarone (also class I, II & IV): 2–5mg/kg over 5min (resus) to 1hr in 5%Dex. (via CVC if poss.) Maint: 15mg/kg in 500ml 5%dex over 24h. Ok in LVF. Long T½.
      1. SE: Proarrhythmic. Long term (vis.dist, photosens, grey skin, abn. LFT/TFT, pulm fibrosis, tremors), unpred effect with warfarin, ↑dig, phenytoin, theophylline levels
  4. Class IV (calcium channel blockers, prolong AV node cond, ↑PR) e.g. verapamil

Brugada Syndrome (See ECG Article for more details)

  1. Cause of sudden cardiac death & 60% of idiopathic VF. Aut.Dom defect in Na channel. More common in Asian males. Ave. age at Dx=30y. ECG features (may be transient) partial RBBB, downsloping ST elevation & ↑or↓T in V1–3. In addition syndrome reqs also one of: syncope, VF, polymorphic VT, FamHx of sudden death<45y, or ST elevation in current family members.

Bradyarrhythmias

Definitions

  1. Strictly: <60bpm in adults, age dependent in children
  2. Relative: too slow for haemodynamic state of patient (may be >60bpm)
  3. Features: If symptoms, may include light-headedness, palpitations, syncope

Types

  1. Sinus bradycardia
    1. Causes:
      1. High resting vagal tone e.g. athletes, young adults
      2. Patients on negative chronotropes
        1. β blockers, CCB, digoxin, amiodarone, theophylline, clonidine
      3. Hypothyroidism
      4. Hypothermia
      5. Cushing reflex (↑ICP)
      6. Bezold-Jarish reflex – parasympathetic stimulation in early inferior MI
      7. Pericardial tamponade
      8. Adrenal insufficiency
      9. Dive reflex in young children (vagal)
      10. Severe jaundice
      11. Pleural/peritoneal stimulation
      12. Rarely carotid hypersensitivity (tight shirt collar) or infection (e.g. typhoid – relative bradycardia)
    2. Management:
      1. Rule out and treat above causes or myocardial ischaemia
      2. If symptomatic (often not until HR<40) treat as below
  2. Ectopic atrial rhythm or wandering atrial pacemaker
    1. Ectopic atrial foci, if >3 foci = wandering atrial pacemaker
    2. Different P wave morphologies PR duration variations
    3. Not normally clinically significant
  3. Sinoatrial (SA) block, sinus exit block or sinus arrest
    1. SA node fails to produce an impulse or not conducted to atria
    2. ECG typically shows absent P waves with escape rhythm
      1. Junctional – narrow complexes @ 40–60bpm, may be accelerated to 60–100
      2. (Idio)Ventricular – wide complexes @ 30–40bpm
    3. Usual causes: Ischaemia, hyperK , vagal tone, negative chronotopes (see above)
    4. Treat if symptomatic
  4. Sick sinus syndrome aka tachy-brady syndrome
    1. Causes: SA/AV nodal fibrosis, ischaemia, CHD, tumours, surgery, cardiomyopathy
    2. ECG may intermittently show SA block, sinus bradycardia or arrest with bursts of atrial tachycardia (usually AF, but also junctional tachycardia, SVT, atrial flutter)
    3. Management:
      1. Treat any symptomatic acute arrhythmia
      2. Most require permanent pacemaker for the bradycardia component & an antiarrhythmic (e.g. digoxin or verapamil) to suppress tachycardias.
  5. AV blocks
    1. First degree
      1. Slow AV node conduction
      2. ECG: PR>200ms
      3. All atrial impulses conducted to ventricles
      4. Benign, but may be assoc with vagal tone, inf MI, digoxin tox, myocarditis
    2. Second degree
      1. Some atrial impulses are not conducted to ventricles
      2. Mobitz type I (Wenckebach)
        1. AV node conduction defect
        2. ECG: Repeated lengthening of PR until a P is not followed by a QRS
        3. Usually asymptomatic and treatment not required
        4. Treat if symptomatic or in context of inferior MI
      3. Mobitz Type II
        1. Conduction defect generally below AV node
        2. Degenerative Lev or Lenegre disease
        3. ECG: constant PR with intermittent QRS absence
          1. Risk of progression to third degree bloc
          2. Atropine often ineffective as block usually below AV node
          3. Permanent pacing is usually required
        4. 2:1 block
        5. 2 P waves per QRS complex. Types I & II indistinguishable on ECG.
        6. May occur in digoxin toxicity or ischaemia
        7. Needs further electrophysiological tests to determine treatment
    3. Third degree
      1. AV dissociation
        1. Atrial impulses not conducted to ventricles
        2. ECG: Both P waves & QRS junctional/escape complexes occur independently
        3. Treat as below – though atropine is unlikely to be effective(unless a nodal block) and a permanent pacemaker will be needed
        4. Myocardial fibrosis is commonest cause
        5. Associations:
          1. Inferior AMI
          2. Sick sinus syndrome
          3. Mobitz type II
          4. Second degree block plus new bundle branch or fascicular block
      2. With all AV blocks additionally rule out
        1. Negative chronotropes (as for sinus bradycardia)
        2. Lyme disease
        3. Myocarditis/endocarditis
        4. SLE
        5. Chagas disease
        6. Myxoedema,
        7. Amyloid
        8. Cardiac surgery/tumours

General Management

  1. ABC, O2
  2. IV access
  3. Bloods: UEC, CMP, Troponin/CK, FBC, TFT or digoxin level as appropriate
  4. ECG
  5. Treat any underlying cause (cease negative chronotrope, correct electrolytes, etc.)
    1. Treat bradycardia only if HR<50 and hypoperfusion (syncope, sysBP <90mmHg, HF)
  6. Drugs:
    1. Atropine: 0.5–1.0mg (0.02mg/kg, minimum of 0.1mg in child) repeated up to 2–3mg
      1. Only useful if increase vagal tone i.e. problem at/above AV node.
    2. Isoprenaline (isoproterenol): bolus 20–40mcg IV, infusion 0.5mcg/min of 2mg/100ml N.Saline
      1. Caution: As a pure beta agonist can cause beta2 vasodilatation in muscle beds leading to hypotension
    3. Adrenaline: infusion 2–10mcg/min
      1. Useful if hypotension an issue. Ideally needs a central line.
    4. Others:
      1. Dopamine: 5–20mcg/kg/min through central line.
      2. Aminophylline
      3. Glucagon (beta blocker/calcium channel OD)
      4. Digoxin Fab (digoxin toxicity)
  7. Pacing:
    1. Temporary if drug therapy fails (likely with Mobitz II 2nd & 3rd degree AV blocks)
      1. Transcutaneous
        1. Via fist (!) or defibrillator pacing function
        2. Will normally require analgesia/sedation
        3. Temporising measure before:
      2. Transvenous wires inserted
    2. Permanent pacemaker

Disposition

  1. Admit to monitored bed if:
    1. Symptomatic
    2. Sick sinus
    3. Mobitz II second degree block
    4. Third degree block

Tachyarrhythmias

  1. Common symptoms: rapÒid palpitations, chest discomfort, dyspnoea.

Types

  1. Narrow complex (QRS ≤ 120ms, origin atrial or nodal)
    1. Regular
      1. Sinus tachycardia
        1. Rates 100 to ~180.
        2. HR variability is maintained unlike SVT.
        3. Causes:
          1. physiological – exercise, anxiety
          2. pharmacological – stimulant use, anticholinergics, β-agonists
          3. pathological – ↑T, ↓Hb, PE, hypoxia, hypovolaemia, myocarditis
      2. Supraventricular tachycardia – see separate article
      3. Atrial flutter – rare in absence of heart disease
        1. Atrial rate ~300, ±2:1 or more AV block. Sawtooth waves: Inf V1.
        2. Causes: IHD (2% of MI), CCF, PE, myocarditis, chest trauma, dig toxic
        3. Rx underlying cond. If unstable DC 25–50J or atrial overdrive pacing (>400bpm). Rate control as for AF. Reversion (amiodarone, flecainide)
      4. Atrial (ectopic) _tachycardia – <10% of SVT. Dig tox. Rx as for AF.
      5. Junctional tachycardia – causes e.g. dig toxic, inf MI, RhF
    2. Irregular
      1. Atrial fibrillation – see separate article
      2. Atrial flutter with variable block
      3. Multifocal atrial tachycardia
        1. 3 atrial foci (diff p wave shapes), HR>100, variable PP, PR, RR ints
        2. Causes: Sev COAD, dig/theophylline tox, large PE, ↓↓O2, DM, sepsis
        3. Mx: Rx underlying cond, electrolytes, Mg2 , metoprolol (?CI in COAD)
  2. Broad complex tachycardias (QRS>120ms, ventricular origin or atrial aberrant cond.)
    1. Regular
      1. Ventricular tachycardia – see separate article
      2. Antidromic AVRT – see SVT article
      3. Narrow complex tachycardia (ST, SVT, A. flutter) with aberrant conduction
    2. Irregular
      1. Torsade de pointes – see VT article
      2. AF with aberrant conduction
      3. _WPW _ _AF – see SVT article
      4. VF
  3. Others
    1. Accelerated junctional tachycardia
      1. Regular narrow complex AV nodal escape rhythm @ 60–100bpm.
    2. Accelerated idioventricular tachycardia
      1. Regular broad complex ectopic rhythm @ 40–110bpm.
      2. Highly specific for myocardial disease e.g. AMI
      3. Only rarely causes haem. instability.
      4. Occ atropine used to increase sinus rate & suppress ectopy.
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