CIRCULATION STUDIO FIELD GUIDE
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Rhythms
All selectable rhythms and their modeled behavior.
Idioventricular Rhythm
Regular wide ventricular complexes with independent atria at 83 bpm. The rate range spans ventricular escape and accelerated idioventricular rhythm; forward flow depends on rate and the underlying condition.
Junctional Rhythm
Narrow QRS with retrograde atrial activation after the QRS in this example. Rate control spans escape, accelerated and junctional tachycardia. Loss of normal AV timing reduces filling efficiency.
Mobitz I (Wenckebach)
Progressive AV delay over three conducted beats, then a blocked P wave (4:3 pattern). Atrial contraction continues through the ventricular pause.
Mobitz II
Two conducted beats retain the same PR interval, then a P wave is blocked. This 3:2 example avoids inferring Mobitz type from 2:1 conduction alone. Bradycardia and pauses reduce perfusion; conduction disease can require pacing.
Monomorphic Ventricular Tachycardia
Monomorphic VT with a pulse: regular wide complexes, independent atrial activity at 83 bpm, and reduced pulse pressure. Pulseless VT is not modeled.
Multifocal Atrial Tachycardia
Irregular atrial rhythm with three P-wave morphologies and variable PR intervals. Often accompanies hypoxia, pulmonary or cardiac disease. Cardioversion does not reliably terminate automatic atrial foci; treat the trigger.
Non-Sustained Ventricular Tachycardia · Atrial Fibrillation Baseline
Irregular AF without discrete P waves between self-terminating 15–20-beat runs of regular monomorphic VT. Runs reduce perfusion, then AF resumes. Ventricular suppression does not imply conversion of the underlying AF.
Non-Sustained Ventricular Tachycardia · Sinus Baseline
Sinus rhythm with self-terminating runs of 15–20 ventricular beats. Rate control sets the baseline rate; VT is 180–240 bpm. Forward stroke volume and arterial/pleth pulses fall during each burst. Amiodarone, lidocaine or metoprolol suppress the runs in this selected teaching response; clinical efficacy is context dependent and no drug kinetics are simulated.
Pacemaker-Mediated Tachycardia
Regular ventricular pacing followed by retrograde P waves that are tracked into the next paced beat. Rapid rate and mistimed atrial contraction reduce output and can raise filling pressures. Device reprogramming is not simulated.
Polymorphic Ventricular Tachycardia
Rapid wide complexes vary in axis and amplitude, with weak variable mechanical pulses. Illustrative perfusing polymorphic VT; no automatic deterioration or long-QT diagnosis is implied.
Pre-Excited Atrial Fibrillation
Irregular rapid ventricular activation with beat-to-beat changes in QRS width, amplitude and fusion, slurred pre-excited upstrokes and secondary repolarization changes. No organized atrial contraction; mechanical pulses vary. Above 120 bpm, the teaching model adds progressively worse filling, lower BP/output and higher wedge pressure, especially with left-heart disease. The size of the response is illustrative, not a universal property of pre-excitation.
Sinus Arrest
Long recurrent absence of P waves and QRS complexes in this selected no-escape example. Real sinus arrest may be followed by an escape rhythm. Pressure runs down and pleth pulses disappear during arrest.
Sinus Arrhythmia
Cyclic sinus RR variability with a consistent P morphology and conducted QRS. A benign pattern alone does not imply shock.
Sinus Pauses
Recurrent sinus pauses interrupt otherwise normally timed P–QRS–T complexes. The rate is the ventricular average over the full repeating sequence; electrical and mechanical pulses stop during the pause.
Sinus Rhythm
Regular atrial contraction precedes each ventricular beat.