Overview

An arrythmia refers to any disturbance in cardiac electrical activity that is not normal sinus rhythm with normal atrioventricular conduction. This may include changes in rate, rhythm or site of origin of the electrical signal for contraction. ¹

Normal conduction of the heart

For the heart to pump normally²:

1. SA node initiates an action potential spreading the current in to the right atrium (RA) and left atrium (LA) via Bachmann’s bundle
2. SA node → AV node
3. AV node delays conduction to ensure ventricles contract AFTER blood is emptied into the ventricles from the atria
4. AV node → Bundle of His
5. Bundle of His → Purkinje Fibres
6. Purkinje fibres → cardiomyocytes (contractile cells)

Classification of Arrythmias

There are numerous types of arrythmias and can be classified as follows:

Supraventricular Arrythmias

Definition: the arrhythmia originates from above the ventricles. Therefore, as the QRS complex represents VENTRICULAR contraction, supraventricular Arrythmias have narrow aka “normal” QRS complexes.

Sinus origin

• Originates from the SA node, therefore has a p-wave before every QRS complex.

Sinus arrythmia

Definition

Sinus arrhythmia is a normal variation of sinus rhythm. It is characterised by an irregular rhythm. More common in younger patients.³

How it works

• Sign of health cardiovascular function
• Resultant from physiological changes in respiration
  • Breathing stimulates the vagus nerve and changes pressures in cardiac filling
  • Vagus nerve has a role in slowing down heart rate

Clinical features

• Usually asymptomatic

ECG features

• P wave before every QRS
  Narrow QRS complex
  Beat-to-beat variation in P-P interval: increasing and decreasing with breathing in and out

Management

• No management

Sinus tachycardia⁴

Definition: >100 bpm in adults, regular rhythm

Causes

• Physiological: exercise, stress, pain
• Pathophysiological
  • Compensation for reduction in stroke volume: e.g., in acute heart failure, myocardial infarction, pulmonary embolism, anaemia, sepsis
  • Increased activation of SNS: e.g., hyperthyroidism, cocaine, amphetamines

Clinical features

• Usually asymptomatic
• Symptomatic: palpitations, dyspnoea, light-headedness, syncope, chest pain

ECG features

• Increased rate
• Nil other abnormalities

Management

• Identify and treat underlying cause. If physiologic, may not need treatment

Sinus bradycardia⁵

Definition: <60 bpm in adults, regular rhythm

Etiology

• Physiological: in athletes, during sleep
• Pathophysiological
  • E.g., Chest trauma, ischemic heart disease, vasovagal stimulation, anti-arrhythmics (e.g., digoxin, adenosine, beta blockers), hypothermia

How it works

• changes in electrical impulse formation, conduction to AV node from SA node, or conduction through to bundle of His/Purkinje fibres.

Clinical features

• Usually asymptomatic
• Symptomatic: fatigue, reduced exercise tolerance, light-headedness, dizziness

ECG features

• Reduced rate <60bpm
• Normal sinus rhythm

Management

• Ensure they are haemodynamically stable, ABCDE approach
• Identify and treat underlying cause

Figure 5: ECG showing Sinus Bradycardia

Sinus arrest⁶

Definition

Delay in the impulse from the SA node for 3 or more seconds, resulting in a skipped beat. Other pacemaker cells (such as those in the AV node) can produce a signal to restart normal rhythm, known as an escape rhythm. If this fails to occur → may lead to cardiac arrest. 

ECG features: absent P waves and contraction for >3 seconds

Management

• ABCDE and haemodynamic assessment
• Address underlying cause
• Holter monitoring
• Consider pacemaker if recurrent

Re-entrant Arrythmias⁷

Definition

Re-entrant Arrythmias is an umbrella term for several tachyArrythmias. A re-entrant circuit refers to a self-sustaining continuous loop of electrical impulse in conductive tissue that has already been stimulated. 

For this to occur, 3 conditions must be met:

• Two adjacent pathways with different conduction velocities and refractory periods:
  • one fast, long refractory period 
  • one other slow, short refractory period
• Adjacent pathways must be connected proximally and distally
• A premature action potential: If the premature action potential occurs when the fast pathway is still in refraction, this allows for a re-entrant circuit to be activated

Paroxysmal Supraventricular tachycardia (PSVT)⁸

Definition

Re-entrant circuit that involves the AV node. Atrioventricular nodal re-entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT) are subtypes with in PSVT.

Triggers

• caffeinated drinks, stress, exercise, nicotine, hyperthyroidism, hypoxia, MI

Clinical features

• Typical: palpitations, fatigue, anxiety, neck fullness
• Other: dizziness, shortness of breath, nausea, chest discomfort

AVNRT vs AVRT

AVNRT9

Two pathways within the AV node (one slow and fast as detailed above) ECG features – tachycardia: often 150-250bpm – narrow QRS – P waves: not visible, or buried in, or just after the QRS complex

AVRT10

Involves the AV node and an accessory (abnormal) pathway outside the AV node which a signal can go from: Atria → ventricle (antidromic) Ventricle → atria (orthodromic) Wolff Parkinson White syndrome: is the most common form of AVRT in which the accessory pathway (Bundle of Kent) allows for orthodromic AVRT. ECG features – Short PR interval (<120ms) – Delta wave: slurring of the first portion of the QRS complex – Widened QRS complex (as a result of the delta wave) – T wave changes to opposite direction of QRS direction https://litfl.com/pre-excitation-syndromes-ecg-library/

Management

• If haemodynamically unstable: e.g., short of breath, hypotensive, chest pain, altered mental status, or in shock → electrical cardioversion immediately
• If stable: first line are vagal manoeuvres: carotid sinus massage or Valsalva
  • If above does not terminate PSVT → adenosine

Atrial Flutter¹¹

Definition: re-entrant circuit around the tricuspid valve, such that the atria are firing at 250-350 bpm. 

How it works: The AV node lacks capacity to let every signal through, creating an AV conduction ratio.

• E.g., for every 3^rd impulse from the atria, 1 goes to the ventricle (3:1 ratio)

Clinical features

• May be asymptomatic
• If symptomatic: palpitations, light-headedness, fatigue, dizziness, syncope, hypotension

ECG features

• Heart rate: variable on the AV ratio.
  • If 3:1 block: usually ~100bpm
  • If 4:1 block: usually ~ 75bpm
• Classic “sawtooth” appearance: in AV ratio

Management¹²

• Often reverts with low energy, direct current electrical cardioversion
• Often atrial flutter is insensitive to anti-arrythmics. However, if cardioversion fails, management is similar to AF (refer to AF management)

Figure 10: Image showing Atrial Flutter

Atrial Fibrillation¹²

Definition: numerous re-entrant circuits within the atria, such that the atria are firing at >500bpm. 

How it works: The AV node lacks capacity to let each signal through, and thus conducts signals at random to the ventricles

Clinical features

• Palpitations, light-headedness, chest discomfort, fatigue, weakness
• Irregular, fast pulse on palpation

ECG features

• Tachycardic
• Irregularly irregular rhythm
• No p-waves
• Occasionally, fibrillatory waves in V1: atria are shaking vigorously

Complication of AF: Increased risk of thromboembolic events (e.g., stroke)

• Pathophysiology: increased stasis of blood within the atria → clot formation → thromboembolism
• Assess stroke risk and bleeding risk
  • A high bleeding risk score does not necessarily mean you do not put them on anticoagulation! 
  • Unless patient has a very low stroke score or very high bleeding risk, anticoagulation therapy for thromboembolism prevention should be used. 

Anticoagulants to use: apixaban, rivaroxaban or dabigatran

Management: split into rhythm or rate control

Rhythm control: generally used for AF diagnosed <12 months, have symptoms despite rate control therapy, or reduced LVEF

• Electrical cardioversion: direct current
• Chemical cardioversion
  • Flecainide: acute or long term rhythm control
  • Amiodarone: acute or long term rhythm control
  • Sotalol: only for long-term rhythm control

Rate control:

• 1^st line: Beta-blockers: atenolol or metoprolol
• 2^nd line: Non-dhp CCBs: diltiazem or verapamil
• Add-on: Digoxin
• If LVEF <40%: amiodarone

Ectopic rhythms

Definition

Heartbeat is initiated by another part of the heart, apart from the SA node (the normal pacemaker). Consequently, extra or skipped beats may occur. This takes the form as premature atrial contraction (PAC) or premature ventricular contraction (PVC).

How it works: these ectopic signals occur prematurely, meaning, before the SA node can fire.

Clinical features

• PAC¹³: mostly asymptomatic. Feeling of skipped beats or palpitations. Shortness of breath, anxiety. Irregular pulse on palpation, skipped or extra beats on auscultation
• PVC¹⁴: mostly asymptomatic. Fatigue, palpitations, light-headedness, dizziness. Irregular pulse on palpation. 

Triggers: Stress, caffeine and alcohol, smoking, electrolyte disturbances

ECG features

Depending on the exact location of the focus, ECG changes will differ drastically. They are transient changes within an otherwise sinus rhythm.

• PAC¹³
  • Normal QRS complex
  • PR interval: may be normal, short or longer than normal
  • P waves: differ in appearance to sinus P waves: may differ in length, shape, height

• PVC¹⁴
  • Premature QRS with abnormal morphology and >120 milliseconds
    • QRS may have LBBB or RBBB appearance depending if ectopic focus is from the right or left ventricle respectively
  • Immediately after abnormal QRS, large T-wave of opposite polarity typically occurs
  • P wave usually missing before abnormal QRS
  • Typically have a compensatory pause after the ectopic beat due to timing of refractory periods between the atria and ventricles

Management

• Typically benign and do not require treatment.
• PACs
  • Avoid triggers of PACs
  • If still recurrent: beta blockers
• PVCs:
  • if recurrent and causing symptoms: beta blockers or calcium channel blockers
  • if triggering ventricular Arrythmias:
    • if currently in ventricular fibrillation: immediate defibrillation
    • consider ablation therapy

Ventricular Arrythmias

Ventricular Tachycardia (VT)¹⁵

Definition

Wide QRS complex tachycardia which originates from an ectopic focus in the ventricles. Defined as ≥3 consecutive beats at a rate of ≥100bpm. This arrhythmia can be life-threatening.

• Sustained VT: lasting ≥30 seconds or becomes haemodynamically unstable within 30 seconds. 
• Non-sustained: < 30 seconds in duration and stays haemodynamically stable. 

Monomorphic vs polymorphic

• Monomorphic VT: each QRS complex, is of the same morphology. Typically due to myocardial scarring from a previous cardiac insult (e.g., myocardial scarring).

• Polymorphic VT: consecutive QRS complexes are not of the same morphology. Commonly due to acute coronary syndrome
  • Torsades de Pointes: a subtype of polymorphic VT which has a classical waxing and waning pattern of QRS complexes. Long QT predisposes people developing Torsades de Pointes.
    • Causes of QT prolongation
      • Electrolyte abnormalities: hypomagnesaemia, hypokalaemia, hypocalcaeima
      • Medications/drugs: anti-arrhythmics, macrolides, olanzapine, haloperidol, TCA antidepressants
      • MI
      • Raised ICP
        

Clinical features

• Syncope, shortness of breath, cardiac arrest, cardiac death

Management

• If in cardiac arrest: start advanced life support (ALS) pathway
• Haemodynamically unstable: direct current cardioversion, if this fails, add IV amiodarone

Ventricular Fibrillation

Definition: wide complex tachycardia with a ventricular rate of >300 bpm. May lead to sudden cardiac death. 

Causes: sustained VT → VF, electrolyte abnormalities, acidosis, hypothermia, cardiomyopathies

How it works: VF occurs when the myocardium in the ventricles depolarise and contracts in an uncoordinated fashion.

Clinical features

• Commonly presents as sudden collapse: no pulse, unconscious
• Pre-event: may have chest pain, shortness of breath, nausea and vomiting

ECG features: wide complex QRS, irregular rhythm. Classical ECG of VF:

Management: follow ALS pathway

Management summary table

References

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