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Module 376 submodulesContemporary electrophysiology and AHA, ACC, and HRS arrhythmia guidance

Arrhythmia Pathophysiology

Connect cardiac action potentials, automaticity, afterdepolarizations, reentry, structural substrate, autonomic and metabolic modulators, and hemodynamic consequences to ECG phenotype and mechanism-directed care.

01

Differentiate fast-response and slow-response action potentials, conduction, refractoriness, and tissue-specific drug effects.

02

Explain enhanced and abnormal automaticity and localize focal impulse generation.

03

Distinguish early from delayed afterdepolarizations and connect each to its clinical triggers.

04

State the conditions required for reentry and apply them to AVNRT, AVRT, flutter, and scar-mediated VT.

05

Integrate structural disease, ischemia, autonomic tone, electrolytes, and genetics into arrhythmia risk.

06

Link mechanism and clinical consequence to electrical therapy, drugs, ablation, devices, anticoagulation, and substrate modification.

37.01

Submodule

Cardiac Action Potentials and Conduction

Fast and slow tissues generate and propagate impulses with different dominant currents, coupling, conduction speeds, and refractory behavior.

What to learn
  • Fast-response phases
  • Nodal pacemaker phases
  • Effective refractory period
  • Conduction velocity and coupling
Cellular electrophysiologyFast-response and slow-response tissues use different currents, conduction velocities, refractory behavior, and drug-sensitive phases.
01Fast tissueSodium-driven phase 0

Atria, ventricles, His-Purkinje

02Slow tissueCalcium-driven phase 0

SA and AV nodes

03RepolarizePotassium currents

Restore excitability

04RefractoryChannel recovery

Limits premature propagation

Separate fast from slow tissue

Atrial, ventricular, and His-Purkinje phase 0 depends on fast sodium influx, while SA and AV nodal phase 0 depends mainly on calcium entry. Potassium currents repolarize both systems. Nodal phase 4 supports spontaneous pacemaker activity.

Connect currents to ECG intervals

Slowing ventricular sodium-dependent conduction can widen QRS. Slowing AV nodal calcium-dependent conduction can prolong PR or block supraventricular impulses. Delaying repolarization can lengthen action potential and QT, but tissue and rate determine the visible effect.

Use refractoriness to explain protection and risk

Effective refractory period limits premature propagation and can interrupt reentry. Channel recovery, membrane voltage, and cycle length matter as much as action-potential duration. A drug can prolong refractoriness in one tissue while producing use-dependent conduction slowing elsewhere.

See slow conduction as double edged

Reduced phase 0 upstroke, ischemic depolarization, fibrosis, and impaired cell coupling slow conduction. Enough slowing can block an impulse, but spatially uneven slowing can allow tissue ahead to recover and facilitate reentry.

Quick check

0 of 1 answered
01Which current primarily drives phase 0 in normal AV nodal cells?
Answer every question to submit.
37.02

Submodule

Automaticity and Ectopic Foci

Impulse formation accelerates when normal pacemakers reach threshold sooner or when injured nonpacemaker tissue acquires spontaneous phase 4 depolarization.

What to learn
  • Enhanced normal automaticity
  • Abnormal automaticity
  • Overdrive suppression
  • Focal localization
Impulse generationEnhanced normal automaticity and abnormal automaticity create focal rhythms when phase 4 slope, threshold, or maximum diastolic potential changes.
01SlopeFaster phase 4 rise

Reach threshold sooner

02ThresholdEasier activation

Increase firing probability

03PotentialLess negative baseline

Alter channel availability

04DriversCatecholamines, ischemia, electrolytes

Correct the substrate

Change time to threshold

Automatic rate rises when phase 4 slope becomes steeper, threshold becomes easier to reach, or maximum diastolic potential becomes less negative. Catecholamines accelerate normal pacemakers, while vagal tone can slow sinus firing and AV conduction.

Distinguish appropriate from abnormal firing

Sinus tachycardia can be a necessary response to fever, hypoxia, hemorrhage, pain, or sepsis. Injured myocardium can develop abnormal automaticity during ischemia, electrolyte disturbance, catecholamine excess, or drug toxicity. Treating the driver is often more important than suppressing rate.

Interpret suppression and escape

A faster pacemaker suppresses slower latent pacemakers. When the dominant rhythm stops, delayed recovery can create a pause followed by atrial, junctional, or ventricular escape. The escape protects perfusion but can also reveal sinus-node or conduction disease.

Use morphology to locate the focus

Focal atrial rhythms alter P-wave morphology. Junctional rhythms often have absent, inverted, or retrograde P waves. Ventricular foci produce wide QRS complexes whose multilead pattern reflects the direction of activation away from the origin.

Quick check

0 of 1 answered
01Why can suppressing sinus tachycardia be harmful in hemorrhage?
Answer every question to submit.
37.03

Submodule

Triggered Activity

Afterdepolarizations require a preceding action potential and arise from prolonged repolarization or intracellular calcium overload.

What to learn
  • Early afterdepolarizations
  • Delayed afterdepolarizations
  • Long-QT torsades
  • Calcium overload and digoxin
Triggered activityAfterdepolarizations depend on a preceding action potential and emerge from repolarization delay or intracellular calcium overload.
01EADDuring phases 2 or 3

Long QT and pause dependence

02DADAfter repolarization

Calcium overload and fast rates

03TriggerCross threshold

Create ectopy or tachycardia

04ControlRemove cause and stabilize

Match therapy to mechanism

Place EADs before repolarization ends

Early afterdepolarizations arise during phases 2 or 3 when action potentials are prolonged and inward currents reactivate. Bradycardia, pauses, low potassium or magnesium, congenital long-QT syndromes, high drug exposure, and interacting QT-active drugs increase risk.

Place DADs after repolarization

Delayed afterdepolarizations occur after phase 3 when intracellular calcium overload triggers spontaneous sarcoplasmic reticulum release and a transient inward current. Catecholamines, rapid rates, ischemia, heart failure, and digoxin can support this mechanism.

Treat torsades as a long-QT mechanism

Torsades is polymorphic VT associated with prolonged QT. Defibrillate sustained unstable episodes, give magnesium for recurrence, correct potassium, remove QT-active causes, and address pause or bradycardia dependence with expert pacing or rate support when needed.

Recognize digoxin's mixed rhythm picture

Digoxin toxicity combines calcium-driven triggered activity with enhanced automaticity and AV nodal suppression, so atrial, junctional, ventricular, and block patterns can coexist. Kidney function, potassium, drug interactions, timing, and clinical severity guide digoxin immune Fab use.

Quick check

0 of 1 answered
01Which mechanism most directly links digoxin toxicity to ventricular ectopy?
Answer every question to submit.
37.04

Submodule

Reentry Circuits

A circulating wavefront becomes self-sustaining when a circuit, one-way block, and sufficiently delayed conduction allow recovered tissue to be activated again.

What to learn
  • Circuit requirements
  • AV nodal reentry
  • Accessory-pathway reentry
  • Scar-mediated ventricular reentry
ReentryReentry requires a circuit, unidirectional block, and conduction slow enough for previously refractory tissue to recover before the impulse returns.
01CircuitAnatomic or functional path

Provide a route

02BlockOne direction fails

Force alternate travel

03DelaySlow conduction

Allow recovery ahead

04InterruptBlock pathway or prolong refractoriness

Terminate the loop

Assemble the reentry conditions

A pathway must permit circulation, one direction must initially block, and the alternate route must conduct slowly enough for tissue ahead to recover. A premature beat often enters during a vulnerable difference in refractoriness and initiates the loop.

Keep AVNRT inside the nodal region

Typical AVNRT uses functionally distinct slow and fast pathways near the AV node. Atrial and ventricular activation can occur nearly together, hiding P waves. Vagal maneuvers and adenosine can terminate stable AV-node-dependent reentry, while ablation can remove a recurrent symptomatic pathway.

Map the accessory pathway in AVRT

AVRT uses the AV node and an accessory atrioventricular connection as circuit limbs. Orthodromic AVRT usually travels down the AV node and returns through the pathway, producing narrow QRS. Preexcited AF is different and can become lethal if AV nodal blockade accelerates accessory conduction.

Find the slow channels within scar

Infarct and cardiomyopathic fibrosis create surviving channels with slow heterogeneous conduction that support monomorphic VT. Acute termination is only one layer. Recurrent-risk care can require ischemia evaluation, antiarrhythmic therapy, ICD protection, and catheter ablation.

Quick check

0 of 1 answered
01Which three conditions are required for classic reentry?
Answer every question to submit.
37.05

Submodule

Structural Substrate and Modulators

Arrhythmia emerges when a trigger meets susceptible tissue shaped by scar, fibrosis, stretch, ischemia, genetics, autonomic tone, metabolic state, and drug exposure.

What to learn
  • Atrial remodeling
  • Scar and ischemia
  • Heart failure and chamber stretch
  • Autonomic, electrolyte, and genetic modifiers
Substrate and triggersFibrosis, scar, chamber stretch, ischemia, genetics, autonomic tone, drugs, and metabolic stress combine to initiate and sustain arrhythmia.
01SubstrateScar, fibrosis, dilation

Create heterogeneity

02TriggerPremature beat or burst

Enter the vulnerable circuit

03ModulatorAutonomic and metabolic state

Change threshold and conduction

04OutcomeBurden and hemodynamics

Determine clinical consequence

Treat AF as progressive atrial disease

Atrial dilation, fibrosis, inflammation, conduction heterogeneity, altered calcium handling, and ectopic triggers sustain AF. Weight, blood pressure, sleep-disordered breathing, alcohol, exercise, tobacco, thyroid disease, and heart failure influence burden and progression.

Link ischemia to triggers and circuits

Ischemia depolarizes cells, alters potassium and calcium handling, slows conduction, increases dispersion, and raises catecholamine tone. Acute ischemia can trigger polymorphic VT or VF, while healed infarct forms a durable monomorphic VT circuit.

Recognize heart-failure remodeling

Pressure and volume load, neurohormonal activation, chamber dilation, fibrosis, and electrolyte-changing therapies increase atrial and ventricular arrhythmia risk. Congestion and perfusion can make a previously tolerated rhythm unstable.

Modify the vulnerable state

Autonomic tone, potassium, magnesium, calcium, acid-base status, temperature, stimulants, drug interactions, and inherited channel or structural variants change trigger threshold and propagation. Correct modifiable factors while evaluating inherited and structural risk when the phenotype demands it.

Quick check

0 of 1 answered
01Which intervention can reduce atrial fibrillation progression beyond simply slowing the ventricular rate?
Answer every question to submit.
37.06

Submodule

Mechanism to Clinical Phenotype

The same mechanism can be tolerated or catastrophic depending on rate, duration, ventricular function, vascular reserve, thromboembolic risk, and downstream perfusion.

What to learn
  • Tachycardia hemodynamics
  • Tachycardia-mediated cardiomyopathy
  • Bradycardia and escape
  • Drugs, ablation, and devices
Mechanism to treatmentRate, rhythm, electrical therapy, ablation, devices, and risk-factor control work at different levels of the arrhythmia system.
01StabilizeRestore perfusion

Electric therapy when unstable

02SuppressAlter channels or autonomic tone

Reduce initiation or maintenance

03EliminateAblate circuit or focus

Modify the substrate

04Prevent harmAnticoagulation and devices

Address downstream risk

Determine whether rate is cause or response

Rapid rhythm shortens filling and coronary perfusion while increasing oxygen demand. Impact depends on rhythm regularity, ventricular function, vascular tone, and duration. The same rate can cause shock in one patient and compensate for sepsis in another.

Look for reversible ventricular dysfunction

Persistent rapid or irregular activation can produce tachycardia-mediated cardiomyopathy. Quantify burden, control the rhythm, use heart-failure therapy, exclude competing causes, and repeat ventricular imaging because recovery supports the diagnosis.

Respect escape rhythms

When sinus impulse formation or AV conduction fails, subsidiary atrial, junctional, or ventricular pacemakers can maintain perfusion. Evaluate cause and stability before suppressing the escape. Pacing provides durable or temporary support when the native system is unreliable.

Match the intervention to the layer

Drugs alter currents, automaticity, conduction, and refractoriness but can be proarrhythmic. Ablation interrupts a focus or circuit. Pacemakers prevent consequences of bradycardia. Defibrillators detect and terminate dangerous ventricular rhythms. Anticoagulation addresses embolic risk rather than rhythm generation.

Quick check

0 of 1 answered
01What is the primary role of an implantable cardioverter-defibrillator?
Answer every question to submit.

Module test

Check the connections.

Each attempt draws 10 questions from the complete 104 question bank.

104 questions in this module bank10 questions per attempt

Each attempt draws a fresh set and rearranges the answer choices.

References

Current clinical foundation.

Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.

  1. American Heart Association. 2025 Adult Advanced Life Support Guidelines
  2. American College of Cardiology. 2023 Atrial Fibrillation Guideline
  3. American College of Cardiology. Supraventricular Tachycardia Guideline Hub
  4. American College of Cardiology. Ventricular Arrhythmias and Sudden Cardiac Death Guideline
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