Atrial Arrhythmias AFIB

Atrial Fibrillation

Guillermo Nimubona Castrillo
Graduate in Medicine · AI Consultant
Editorial track:

Technical model documentation. Not reviewed by a cardiology specialist.

Last technical review:

Also known as: Atrial Fibrillation · fibrilacion auricular · fibrilación auricular · FA · ACxFA · arritmia completa por fibrilacion auricular · atrial fibrillation · AF · afib

What this page documents

This page details the bioelectrical architecture, mathematical constants of chaotic atrial depolarization, and atrioventricular node behavior parameterized in the MioAtlas three-dimensional cardiac simulator for atrial fibrillation. The sole purpose of this document is to provide transparency regarding computational modeling and its biophysical foundations; it does not constitute clinical practice guidelines, emergency protocols, or a medical diagnostic tool. For an in-depth description of the mathematical integration of the 12 leads, refer to the technical methodology section.

Model parameters

The quantitative values governing atrial excitation kinematics and ventricular response in the simulation engine derive from the AFIB entity configuration in the conduction system catalog:

Parameter Engine value Unit Computational biophysical description
mechanism reentrada — Multiple disorganized wavefronts colliding and fragmenting across both atria.
origin.focus FOCUS_LA_PV — Triggering ectopic focus anatomically anchored in the ostium of the left pulmonary veins.
atrialRate 450 bpm Intrinsic atrial micro-undulation rate (high-frequency oscillatory f waves).
chaos.waveletCount 7 wavelets Number of simultaneous independent reentrant wavelets simulated on the atrial mesh.
rate.default 125 bpm Baseline mean ventricular rate with uncontrolled pharmacologic ventricular response.
rate.range 90 – 170 bpm Physiological variability range admissible under interactive modulation in the simulator.
regularity irregular — Complete arrhythmia; stochastic activation cadence of the atrioventricular node.
rrVariationPercent 40 % Pseudorandom percentage dispersion applied to the R-R interval calculation between consecutive cycles.
pWave fibrillatory — Absence of discrete P deflection; continuous synthesis of low-voltage baseline undulation.
prMs null ms Undefined PR interval due to the lack of unified sinus depolarization prior to the QRS.
qrsMs 90 ms Duration of narrow ventricular depolarization with intact His-Purkinje conduction.
qrsMorphology normal — Physiological ventricular vectorcardiography without associated bundle branch defects.
avConduction.type variable — Probabilistic filtering of the AV node dependent on the relative functional refractory period.
keyLeads V1, II — Leads with maximum visual sensitivity for analyzing f-wave voltage and R-R cadence.

Source of each parameter value

The bioelectrical parameterization implemented in MioAtlas is grounded in the following peer-reviewed scientific sources:

  1. Anatomical localization of ectopic trigger (FOCUS_LA_PV): Assignment of the initial focus to myocardial sleeves of the pulmonary veins matches classic atrial microanatomy described by Anderson et al. (2009).
  2. 12-lead ECG tracing generation and calibration standards: Recording speed at 25 mm/s, voltage calibration at 10 mm/mV, and narrow QRS complex morphology (90 ms) follow AHA/ACCF/HRS standardization guidelines in Kligfield et al. (2007).
  3. Dipole dynamics and 3D ECG synthesis: Wavefront propagation using multiple spatial dipoles projected onto a synthetic torso is based on the whole-heart electrical activity model by Sovilj et al. (2013).
  4. Dynamic QT interval adaptation: Despite R-R cycle irregularity, theoretical ventricular repolarization duration dynamically adjusts cycle-by-cycle using the cubic formula of Fridericia (1920).

How it is modeled

In the interactive coronal cut of the heart, the simulator decouples sinus activity from the SA node and instantiates a multifrequency noise generator across the left and right atria. This generator decomposes atrial activity into 7 micro-reentrant wavelets (waveletCount = 7) propagating across the myocardial mesh with heterogeneous conduction velocity.

At the atrioventricular junction, the AV node is modeled as a probabilistic refractory state filter. When a wavelet reaches the node, the algorithm evaluates the elapsed time since the preceding ventricular depolarization; if the node is in its absolute refractory phase, the impulse is blocked; if in the relative refractory phase, a variable latency is introduced before propagating the action potential down the bundle of His. The resulting 12-lead ECG demonstrates an absence of P waves, replaced by low-amplitude f waves (0.05 – 0.15 mV) and completely irregular R-R intervals with up to 40% dispersion.

What is NOT reproduced

To maintain smooth rendering at 120 frames per second in the browser without excessive CPU overhead, the model incorporates deliberate biophysical simplifications:

  • Intracavity hemodynamics and loss of atrial kick: The simulator does not calculate real-time reductions in cardiac output or left ventricular end-diastolic pressure variations resulting from the loss of coordinated mechanical atrial systole.
  • Thrombogenesis and blood stasis risk: Computational fluid dynamics (CFD) of left atrial appendage stasis and automated embolic risk scoring are not implemented.
  • Adaptive autonomic tone: Sympathetic and parasympathetic tone fluctuations are not dynamically recalculated for postural changes or stress, remaining within static user-selected bounds.
  • Beat-to-beat Ashman phenomenon: Although R-R intervals are irregular, the simulator does not automatically generate transient right bundle aberrancy following a long-short cycle sequence unless explicitly configured.
  • Detailed cellular electrophysiology: Individual membrane ionic currents (IKur, INa, ICaL) via high-density Hodgkin-Huxley formulations are omitted.

Interactive variants

You can inspect different bioelectrical setups and associated conditions directly in the simulator via these deep links:

To explore supraventricular rhythm disturbances and activation pathways in the 3D environment:

Related clinical comparisons

Sources and bibliographic references

  1. Anderson RH, Yanni J, Boyett MR, Chandler NJ, Dobrzynski H (2009). "The anatomy of the cardiac conduction system". Clin Anat.
  2. Kligfield P, Gettes LS, Bailey JJ, et al. (2007). "Recommendations for the standardization and interpretation of the electrocardiogram: Part I: The electrocardiogram and its technology". Circulation.
  3. Sovilj S, Magjarević R, Lovell NH, Dokos S (2013). "A simplified 3D model of whole heart electrical activity and 12-lead ECG generation". Comput Math Methods Med.
  4. Fridericia LS (1920). "Die Systolendauer im Elektrokardiogramm bei normalen Menschen und bei Herzkranken". Acta Med Scand.