Scrub Notes | Cardiac Battery & Electrophysiology Lab

Interactive controls

1) Scroll through one heartbeat

Explore six consecutive beats. Select a beat and scrub its timeline; the ECG, conduction light, chamber contraction and blood movement stay synchronized. A skipped ventricular beat has no QRS and no ventricular contraction.

Selected beat within the rhythm

Beat 1 · Normal conduction

Beat position

SA node fires0%Diastolic refill

Playback speed

2) Electrolyte sliders

These are conceptual physiology controls, not serum laboratory measurements. Magnesium is pictured as a stabilizing battery case (an analogy, not anatomical membrane structure). Sodium-channel current drives working-ventricular-cell phase 0; potassium influences resting voltage and repolarization; calcium supports the plateau and contraction.

Fast sodium-channel current (Na⁺)

LowNormalHigh

Extracellular potassium influence (K⁺)

LowNormalHigh

Calcium influence (Ca²⁺)

LowNormalHigh

Magnesium influence (Mg²⁺)

LowNormalHigh

3) Conduction changes

Heart block / conduction pattern Pacemaker

How to think about it: first-degree block delays every P→QRS; Mobitz I lengthens PR until a P is dropped; Mobitz II drops QRS with otherwise fixed PR; complete block creates P–QRS dissociation. Atrial-only pacing cannot bypass a serious AV block; ventricular and dual-chamber pacing can supply ventricular activation. This model assumes reliable pacemaker capture.

4) What to watch for

Does the light pulse move smoothly from SA → AV → His → Purkinje?
Do the atria contract before the ventricles?
Do the oxygenated and deoxygenated blood paths stay visually distinct?
How do electrolyte changes alter the ECG, contraction strength, and repolarization timing?
Which part of the cycle is being affected most: depolarization, conduction delay, plateau, repolarization, or mechanical contraction?

Anatomical pathway + mechanical heart response

Phase

0–10%

Legend

Color key

Deoxygenated blood

Oxygenated blood

Conduction tissue / impulse

Magnesium = stabilizing housing

Sodium = fast depolarization

Potassium = repolarization / resting potential

Calcium = plateau + contraction

Pacemaker spike / artificial trigger

Battery model

The magnesium shell is a mnemonic for electrical stability, not the literal membrane. Magnesium deficiency can accompany low potassium and increase susceptibility to triggered rhythms, particularly when repolarization is prolonged.

Live ECG strip

Yellow cursor = current moment in the selected beat.

Clinical interpretation panel

Primary ECG changeNormal conduction and morphology.

Electrolyte teaching pointBalanced ions support coordinated depolarization, repolarization, and contraction.

Conduction statusImpulse travels SA → AV → His → bundle branches → Purkinje.

Mechanical effectAtria contract first, then ventricles eject blood in sequence.

Why this matters: Electrolytes influence automaticity, conduction velocity, action potential shape, repolarization, and contractility. The strip is only one part of the story — the tissue behavior underneath explains the waveform.

Model limitations: Schematic, intentionally not drawn to anatomical scale. ECG shapes are generated for education; morphology varies between real patients. Ion-control values are dimensionless and cannot diagnose electrolyte concentrations; low blood sodium alone does not predict the ventricular QRS change shown for fast sodium-channel current. A pacemaker mode assumes capture and simplified timing. PEA, fusion beats and sensing/capture failures are outside this model.

Independent educational references: MedlinePlus: Cardiac conduction (2026) NCBI Bookshelf: AV block NCBI Bookshelf: Hypokalemia Open RN: AV block table (CC BY 4.0)

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