Pathophysiology of a Functional Rhythm
A functional rhythm occurs when structural and/or electrophysiological abnormalities alter cardiac tissue to promote abnormal impulse formation and/or propagation, resulting in a rhythm that emerges as a backup pacemaker when higher pacemakers fail. 1
Mechanisms of Functional Rhythms
Functional rhythms typically arise through one of three primary mechanisms: abnormal automaticity, triggered activity, or re-entry 1
Abnormal automaticity: Occurs when cells with enhanced diastolic phase 4 depolarization increase their firing rate compared to normal pacemaker cells, potentially overdriving the sinus node and becoming the predominant pacemaker 1
Triggered activity: Associated with disturbances of repolarization where afterdepolarizations of sufficient magnitude reach threshold and trigger early action potentials during the repolarization phase 1
Re-entry: The most common arrhythmia mechanism, involving repetitive excitation of a region of the heart due to conduction of an electrical impulse around a fixed obstacle in a defined circuit 1
Pathophysiological Requirements for Re-entrant Functional Rhythms
Initiation requires unidirectional conduction block in one limb of a circuit, which may occur from acceleration of heart rate or block of a premature impulse that encounters refractory tissue 1
Slow conduction is usually necessary for both initiation and maintenance of a circus movement tachycardia 1
In functionally determined re-entry, propagation occurs through relatively refractory tissue with an absence of a fully excitable gap 1
Structural and Electrophysiological Substrates
Any disturbance of cardiac architecture potentially increases susceptibility to functional rhythms 1
Common structural changes include inflammation, fibrosis, hypertrophy, which often occur with underlying heart disease such as hypertension, coronary artery disease, valvular heart disease, and heart failure 1
These conditions tend to increase chamber pressure, cause dilation, and alter wall stress, creating the substrate for functional rhythms 1
Myocardial fibrosis is a common feature in both experimental and clinical arrhythmias, with atria being more sensitive to profibrotic signaling than ventricles 1
Prolonged rapid pacing can increase arrhythmia susceptibility by causing myocyte loss, mitochondrial disturbances, and gap-junction abnormalities leading to cell necrosis and apoptosis 1
Specialized Conduction Tissues and Heterogeneity
The sinoatrial node, atria, and atrioventricular node are heterogeneous structures with distinct electrophysiological specialization of tissues and cells 1
Cellular heterogeneity is a prominent feature in nodal tissues, with the central portion of the sinus node containing cells with longer action potentials and faster rates of phase 4 diastolic depolarization 1
Differences in ion channel expression underlie the electrophysiological behavior variations between cell types in the conduction system 1
Time-Dependent Factors
Circadian mechanisms govern cardiac rhythms and susceptibility to arrhythmia, with circadian clocks within the brain and heart setting daily rhythms in sinoatrial and atrioventricular node activity 2
The balance of circadian inputs from the autonomic nervous system and cardiomyocyte clocks to the SA and AV nodes differ, potentially rendering the cardiac conduction system sensitive to decoupling during abrupt shifts in behavioral routine 2
Clinical Implications and Manifestations
Functional rhythms can present with various symptoms including palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, or presyncope 1
The presence of functional rhythms may be associated with worse New York Heart Association Functional Class (NYHA-FC) 3
In patients with structural heart disease, the most common abnormality identified during electrophysiological testing is induction of sustained monomorphic ventricular tachycardia 1
Left atrial hypertension, electrical conduction slowing, and mechanical dysfunction form a pathophysiological triad associated with atrial cardiomyopathy and increased arrhythmia recurrence 4
Therapeutic Considerations
Understanding the specific mechanism of a functional rhythm is essential for appropriate therapeutic intervention 1
Electrical treatment approaches may reverse or mitigate heart failure associated with functional rhythms, including ablation therapies and cardiac resynchronization therapy 5
Termination by vagal maneuvers suggests a re-entrant tachycardia involving AV nodal tissue 1