Summary Part 4 - ARRHYTHMIAS

The normal resting heart rate in adults is 50-100 bpm, with respiratory variation.

  1. Block and bradycardia
    • Pauses of ≥3 seconds may be clinically relevant. Sinus bradycardia in the well trained may be as slow as 30 bpm. If the sinus node fails to stimulate, pacemaker cells from lower parts of the conduction system may generate escape beats, but often disease processes may affect the entire conduction system
    • Sinus arrest: The sinus node fails for a while, and there is no normal P wave
    • Sino-atrial block (SA block): The sinus node generates impulses, but these do not reach atrial cells. The P wave is missing, but returns after an interval of one or more normal P-P intervals
    • First degree AV -block is not a true block, but merely delayed conduction; all impulses are conducted, but the PQ interval is ≥0.22, usually without any clinical consequence. In 2nd degree AV block grad 2 one QRS complex is missing. In 2nd degree (Wenckebach) block (also called Mobitz type 1) the PQ interval is first normal, then increasing with each beat until a dropped QRS complex, and then the sequence repeats. This is regarded as harmless, whereas in Mobitz type 2 block, a random QRS is blocked, signifying a diseased conduction system, and an implanted pacemaker is usually recommended. In complete AV block (3rd degree) no P waves are conducted, and atria and ventricles beat independently. Intermittent AV block often causes syncope (Stokes-Adams attacks) or cardiac arrest. Pacemaker treatment is indicated in AV-blokk of 2nd degree (Mobitz type 2) and grade 3
  2. Premature beats
    • In the absence of bundle branch block premature supraventricular beats have narrow QRS complexes, whereas those of ventricular origin lack the P wave and are wide. Occasionally they may cause a retrograde P wave that sometimes is visible, or is recognized only by its reset of the sinus node, causing a delayed next P wave. One premature beat in a 10 s recording amounts to 8640/24 h if representative. Premature beats are not dangerous, but a large number of premature supraventricular beats associates with increased risk of atrial fibrillation, and abundant VPBs may indicate, and even trigger heart failure.
  3. Supraventricular tachycardias (SVT)
    • Paroxysmal supraventricular tachycardias may occur in otherwise healthy hearts. They use to have a sudden onset, abrupt termination and a regular rate. Reentry is the common mechanism for the arrhythmia, mainly in the AV node (AVNRT), or atria and ventricles both participate in the arrhythmic circuit through both an AV nodal and an accessory bundle connection (AVRT, or WPW syndrome). Atrial tachycardia is the least prevalent SVT, and it is caused either by reentry or triggered automatism. All SVTs are amenable to cure by catheter ablation.
    • In atrial flutter we typically see regular flutter waves at a rate of 220-300 bpm, usually from the right atrium or around scar tissue. Fortunately, the AV node blocks one half or more of these impulses (2:1, 3:1 or variable conduction).
    • In atrial fibrillation only parts of the atrial walls depolarize synchronously, and the fibrillatory waves appear at a rate of 350+/min. Typically, the conducted beats are irregular
  4. Ventricular tachycardias (VT)
    • In VT the ventricles run away independent of atrial activity. Usually there are more QRS complexes than there are P waves. The QRS complexes are wide. A longs strip of ECG lead II is often useful in the search for P waves. An occasional less broad QRS may often be seen, representing ventricular capture by a normally conducted beat, or fusion beats, with elements from both normal and ventricular origin. A regular VT usually is a reentry tachycardia, around or within a scar area, and usually signifies serious heart disease. VT may degenerate to VF/heart arrest. In some cases the arrhythmic mechanism can be destroyed by catheter ablation, but often should an ICD be used as a safety net.
    • Polymorphic VT is also called torsades de pointes: The QT interval is usually prolonged, and the QRS complexes are fast and irregular with a systematic change in axis and morphology. The arrhythmic mechanism is usually triggered automatism from cells that are filled with calcium, and therefore generate afterdepolarizations that trigger premature beats that initiate VT and fibrillation.