Arrythmias

Overview

An arrhythmia 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

Sinoatrial (SA) Node Arrhythmias Upright P waves all look similar. PR intervals and QRS complexes are of normal duration

• Sinus Bradycardia
• Sinus Tachycardia
• Sinus Pause (Sinus Arrest)
• Sinoatrial (SA) Block

Atrial arrythmias P Waves differ in appearance from sinus P waves. QRS Complexes are of normal duration

• Atrial Tachycardia
• Supraventricular Tachycardia (SVT)
  • Paroxysmal Supraventricular Tachycardia (PSVT)
  • Atrial Fibrillation (A-fib)
  • Atrial Flutter (A-flutter)
  • Wolff-Parkinson-White (WPW) Syndrome

Junctional Arrhythmias The atria and SA node do not perform their normal pacemaking functions. A junctional escape rhythm begins.

• Junctional Rhythm
• Accelerated Junctional Rhythm
• Junctional Tachycardia

Ventricular arrythmias These arrhythmias start in the heart's lower chambers, the ventricles. This is life-threatening. QRS complex is 0.10 sec. P Waves are absent or, if visible, have no consistent relationship to the QRS complex.

• Premature Ventricular Contraction (PVC)
• Ventricular tachycardia
• Ventricular fibrillation
• Torsade de Pointes
• Asystole

Atrioventricular (AV) Blocks AV blocks are divided into three categories: first-, second-, and third-degree

• First-Degree AV Block
• Second-Degree AV Block (Type I and Type II)
• Third-Degree AV Block

Bundle Branch blocks

• Bundle Branch Block

ST elevation indicates transmural ischaemia

Long QT Syndrome

Wolff Parkinson's White Syndrome

Overview

An accessory conduction pathway is present between the atria and the ventricles. Electrical impulses are rapidly conducted to the ventricles. These rapid impulses create slurring of the initial portion of the QRS called the delta wave.

• WPW is a atrioventricular reentry tachycardia (AVRT)

ECG changes

• Delta Wave
• Shortned PR interval
• Tachycardia >150bpm

Ventricular tachycardia

Overview 

VT or PVT (paroxysmal VT) is produced by a very irritable ventricular focus that suddenly paces in the 150-250 bpm range. Therefore there is a trigger of making the focus irritable. Remember the SA node still paces the atria so VT is a type of AV dissociation when you think about it!

Triggers

• ↓Oxygen
  • Airway obstruction
  • Absence of air - drowning
  • Air with poor O2 content
  • Minimal blood oxygenation in lungs - PE, pneumothorax
  • Reduced cardiac output - shock
  • Poor to absent coronary artery supply
• ↓Potassium
• Pathology
  • Mitral valve prolpase
  • Myocarditis

ECG features

• Widened QRS
• Differentiate between SVT specifically AVRT
  • Presence of captures or fusion confirms VT because this does not occur in SVT!

Management of Pulseless VT

• Advanced Life Support Algorithm

Management of Stable VT

• Controversial
• Amiodarone 300mg IV over 30-60min then 900 over 24h OR Cardioversion

Management of Unstable VT

• ABC
• Oxygen
• ECG and bloods
• IV access
• Identify and treat reversible causes
• Then
  • Synchronised DC shock (up to 3 attempts)
  • Amiodarone 300 mg IV over 10-20 minutes
  • Repeat shock
  • Then give amidarone 900 over 24h

Remember It is important to confirm the presence or absence of pulses because monomorphic VT may be perfusing or nonperfusing.

Remember Monomorphic VT will probably deteriorate into VF or unstable VT if sustained and not treated.

Torsades de Pointes (twisting of points)

Overview

Torsades is a type of VT characterised by a twisted ribbon appearnece on ECG. TdP is often short lived and self terminating, however can be associated with hemodynamic instability and collapse. TdP may also degenerate into ventricular fibrillation.

Aetiology

• ↓Potassium
• Medication that block the potassium channel
• Congenital abnormalities (long QT syndrome) all of which lengthen the QT segment.

ECG findings

• During short runs of TdP or single lead recording the characteristic “twisting” morphology may not be apparent.
• Bigeminy in a patient with a known long QT syndrome may herald imminent TdP.
• TdP with heart rates > 220 beats/min are of longer duration and more likely to degenerate into VF.
• Presence of abnormal (“giant”) T-U waves may precede TdP

Management

• Magnesium sulphate
• Isoprenaline
• Overdrive pacing

Ventricular Fibrillation

Overview

VF is caused by rapid rate discharge from many irritable parasystolic automaticity foci, producing an erratic, rapid twitching of ventricles (ventricular rate is 350-450 bpm). Because there are so many foci, many small areas of ventricule depolarize causing ineffective twitching of the ventricles → ↓cardiac output.

• Ventricular fibrillation (VF) is the the most important shockable cardiac arrest rhythm.
• There is no effective cardiac output, because the ventricles are only twitching erratically.
• Unless advanced life support is rapidly instituted, this rhythm is invariably fatal.

ECG findings

• Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration (coarse VF -> fine VF)

Mechanism

• Premature ventricular contractions (PVCs)
• ST changes
• R on T phenomenon
• Pauses
• QT prolongation
• Ventricular tachycardia
• Supraventricular arrhythmias
• Sinus tachycardia

Atrioventricular Blocks

ICD

Overview 

Ventricular fibrillation (VF) is a common cause of sudden cardiac death (SCD) and is sometimes preceded by monomorphic or polymorphic ventricular tachycardia (VT). Although cardiopulmonary resuscitation, including chest compressions and assisted ventilation, can provide transient circulatory support for the patient with cardiac arrest, the only effective approach for terminating VF is electrical defibrillation. Success with external defibrillation led to the development of an implantable defibrillator in the mid-1960s.

Indications

• Primary prevention
  • History of MI with left ventricular ejection fraction <30
  • Cardiomyopathy class II-III with left ventricular ejection fraction <35
  • Syncope due to structural heart disease and inducible sustained VT or VT going to VF on electrophysiology study
  • Other high risk
    • Long-QT syndrome
    • Hypertrophic cardiomyopathy
    • Brugada syndrome
    • Arrthmogenic right ventricular cardiomayopathy
• Secondary prevention
  • Previous resuscitated VT/VF
  • Previous episodes of VT with evidence of heart disease

Contraindications

• Reversible VT (drug, electrolyte)
• VF or VT amenable to surgical or catheter ablation
  • WPW
• Poor survival
• Significant psychiatric illness
• Heart failure NYHA IV
• Syncope without inducible ventricular tachyarrhythmias and without structural heart disease

References