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[ Home ](https://mdster.com) 2. [ Blog ](https://mdster.com/blog) 3. [ Medical Education ](https://mdster.com/blog?category=medical-education) 4. ECG Electrophysiology Basics for the ED: Phases, Nodes, Mechanisms [ Medical Education ](https://mdster.com/blog?category=medical-education) ECG Electrophysiology Basics for the ED: Phases, Nodes, Mechanisms ==================================================================== A practical Emergency Medicine review of action potentials, AV nodal physiology, His-Purkinje conduction, and the three mechanisms behind tachyarrhythmias. [ MDster Editorial Team ](https://mdster.com/about) · Mar 17, 2026 · 7 min read · 148 [ Reviewed by Dr. Ali Ragab, MBBCH, MSc, MCAI ](https://mdster.com/medical-reviewers/dr-ali-ragab) [Editorial Policy](https://mdster.com/editorial-policy) | [Corrections Policy](https://mdster.com/corrections) [ Board Review ](https://mdster.com/blog?tag=board-review) [ Emergency Medicine ](https://mdster.com/blog?tag=emergency-medicine) [ Cardiovascular Physiology ](https://mdster.com/blog?tag=cardiovascular-physiology) [ ECG ](https://mdster.com/blog?tag=ecg) [ Arrhythmias ](https://mdster.com/blog?tag=arrhythmias) Share this article Share this post At 2 a.m. the monitor shows a regular tachycardia at 190, and somebody says, just push adenosine. Sometimes that is exactly right. Sometimes it only unmasks flutter. Sometimes it is the wrong reflex entirely. The difference is electrophysiology: what tissue generated the impulse, what tissue is sustaining it, and which ion current the rhythm depends on. If you can map the ECG back to the cell, drug choice becomes logic instead of folklore. [\[1\]](#cite-1 "Reference [1]") Start With the Action Potential ------------------------------- Start by separating **fast-response** tissue from **slow-response** tissue. Atrial myocardium, ventricular myocardium, and the **His-Purkinje system** are fast-response tissues: **phase 0** is fast Na influx, **phase 1** is early repolarization, **phase 2** is the Ca-mediated plateau balanced by K efflux, **phase 3** is K-dominant repolarization, and **phase 4** is a stable resting potential maintained largely by inward-rectifier K current. On the ECG, the **QRS** reflects ventricular phase 0, the **ST segment** tracks the plateau, and the **T wave** tracks ventricular repolarization. [\[2\]](#cite-2 "Reference [2]") The **AV node** plays by different rules. Nodal tissue has a **slow-response** action potential: its phase 0 depends mainly on **L-type Ca channels**, its phase 4 is not flat, and automaticity is shaped by funny current and autonomic tone. That is why the drugs behave the way they do. **Adenosine**, **beta-blockers**, **diltiazem**, and **verapamil** work because they slow Ca-dependent nodal conduction or increase nodal refractoriness. **Class I** agents target fast Na-dependent tissue and show **use dependence**, so QRS widening becomes more obvious at higher rates. **Class III** agents prolong action potential duration and effective refractory period by blocking repolarizing K currents, but pure K blockers are prone to **reverse use dependence**, so QT prolongation can be worse at slow rates or after pauses. [\[3\]](#cite-3 "Reference [3]") > **Clinical Pearl:** **Adenosine is a nodal probe, not a cure-all.** If a tachycardia stops, the AV node was part of the circuit; if flutter waves appear, you learned the mechanism without fixing the atrial rhythm. [\[1\]](#cite-1 "Reference [1]") AV Node vs His-Purkinje: Why This Changes the ECG ------------------------------------------------- This is the comparison that explains a lot of board questions and a lot of bedside mistakes. [\[4\]](#cite-4 "Reference [4]") FeatureAV nodeHis-Purkinje systemDominant phase 0 currentL-type CaFast NaConduction behaviorSlow, decremental, autonomically sensitiveVery rapid, relatively all-or-noneTypical ECG impactPR delayRapid ventricular activation, QRS morphologyCommon ED implicationAVNRT responds to nodal blockadeFascicular/bundle VT can mimic SVT The **PR interval** is mostly **AV nodal delay**, not His-Purkinje delay. The AV node conducts slowly and decrementally; published estimates put nodal-region conduction around **0.02-0.1 m/s**, versus roughly **1.2-1.7 m/s** in the His bundle and **3-4 m/s** in Purkinje tissue. That is why Wenckebach is nodal, why nodal blockers terminate **AVNRT**, and why disease in fast tissue widens the **QRS** instead of merely lengthening the PR. It also explains the classic trap of **verapamil-sensitive fascicular VT**: the rhythm may be organized and even relatively narrow, but the mechanism lives in specialized ventricular conduction tissue, not in the AV node. [\[4\]](#cite-4 "Reference [4]") Reentry, Automaticity, and Triggered Activity --------------------------------------------- Almost every tachyarrhythmia question reduces to three mechanisms: **reentry**, **automaticity**, or **triggered activity**. Do not memorize names only; ask what keeps the rhythm going. [\[5\]](#cite-5 "Reference [5]") **Reentry** is the workhorse of emergency arrhythmias. It needs **unidirectional block**, sufficiently **slow conduction**, and excitable tissue ahead of the wavefront. That combination makes **abrupt onset and abrupt termination** the classic bedside clue. **AVNRT**, **orthodromic AVRT**, typical flutter, scar VT, and many fascicular VTs are reentrant. Reentry loves substrate: scar, ischemia, fibrosis, bundle disease, or any physiology that shortens wavelength by slowing conduction or altering refractoriness. It also explains why synchronized cardioversion works so reliably: break the loop and the rhythm stops. [\[6\]](#cite-6 "Reference [6]") **Automaticity** is spontaneous impulse generation from abnormal **phase 4 depolarization**. Think sinus tachycardia, ectopic atrial tachycardia, and **accelerated idioventricular rhythm** rather than classic paroxysmal SVT. The clues are **warm-up and cool-down** behavior, catecholamine sensitivity, and failure of adenosine to truly terminate an atrial focus even if it transiently blocks AV conduction and exposes the atrial activity. In the ED, treat the driver: ischemia, hypoxia, pain, sepsis, stimulant exposure, or excess sympathetic tone. [\[7\]](#cite-7 "Reference [7]") **Triggered activity** needs a preceding beat. **EADs** occur before full repolarization, usually in **phase 2 or phase 3**, and are classically associated with prolonged action potentials and long-QT states; that is your **pause-dependent torsades** physiology. **DADs** occur after full repolarization in **phase 4** and reflect intracellular Ca overload; think **digoxin toxicity**, catecholamine excess, CPVT, or reperfusion-type ectopy. This distinction matters because the treatment logic changes. EAD physiology pushes you toward magnesium, stopping QT-prolonging drugs, correcting K, and sometimes increasing the heart rate. DAD physiology pushes you toward reducing catecholamine drive and Ca overload, often with beta-blockade and treatment of the underlying trigger. [\[7\]](#cite-7 "Reference [7]") Clinical Correlations in Emergency Medicine ------------------------------------------- In practice, think **mechanism first, label second**. A **regular narrow-complex tachycardia** is usually AV-node dependent until proven otherwise, so vagal maneuvers and adenosine make physiologic sense. A **regular monomorphic wide-complex tachycardia** may still permit adenosine if the patient is stable and the diagnosis is uncertain, but the **2025 AHA ALS guidance** limits that to selected regular monomorphic rhythms and specifically advises against adenosine in **unstable**, **irregularly irregular**, or **polymorphic** wide-complex tachycardia; **verapamil and diltiazem should not be given** to undifferentiated wide-complex tachycardia. That is not algorithm worship. It is mechanism-based medicine: nodal blockers treat nodal tissue, not ventricular sodium-channel disease or pre-excited chaos. [\[1\]](#cite-1 "Reference [1]") One last exam trap: a rhythm can show more than one mechanism. A **Purkinje PVC** may be triggered activity, then fall into vulnerable tissue and start **reentry**. **Atrial flutter** is reentry, but the ventricular rate you see is filtered by the **AV node**. So adenosine may diagnose without curing. If you remember that every ECG is the surface expression of **impulse generation + impulse propagation + refractoriness**, difficult tracings become much less mysterious. [\[5\]](#cite-5 "Reference [5]") Key Takeaways ------------- - **Fast-response tissue** is myocardium and His-Purkinje; **slow-response tissue** is nodal. QRS problems are usually fast-tissue problems. [\[8\]](#cite-8 "Reference [8]") - **Class I** drugs target Na-dependent phase 0 and often widen QRS at higher rates; **adenosine/Class IV** drugs target the AV node; **Class III** drugs prolong repolarization and can worsen QT at slow rates. [\[3\]](#cite-3 "Reference [3]") - **Reentry** is abrupt on/off; **automaticity** warms up and cools down; **triggered activity** follows afterdepolarizations. [\[6\]](#cite-6 "Reference [6]") - **PR prolongation** is mainly nodal; very rapid ventricular activation depends on the **His-Purkinje system**. [\[9\]](#cite-9 "Reference [9]") - In the ED, do **not** give AV nodal blockers to undifferentiated wide-complex tachycardia; adenosine has a role only in selected regular rhythms. [\[1\]](#cite-1 "Reference [1]") Conclusion ---------- ECG electrophysiology is not abstract basic science. It is the reason one drug terminates AVNRT, another widens the QRS, and a pause before a polymorphic beat should make you think torsades immediately. Learn the tissue, the ion current, and the mechanism. The ECG will start to read like physiology instead of pattern recognition alone. [\[8\]](#cite-8 "Reference [8]") References (15) ------------------- 1. 1. [ cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/adult-advanced-life-support ](https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/adult-advanced-life-support) [↩](#cite-ref-1-1 "Back to text") 2. 2. [ pmc.ncbi.nlm.nih.gov/articles/PMC12207207 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC12207207/) [↩](#cite-ref-2-1 "Back to text") 3. 3. [ pmc.ncbi.nlm.nih.gov/articles/PMC12367031 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC12367031/) [↩](#cite-ref-3-1 "Back to text") 4. 4. [ pmc.ncbi.nlm.nih.gov/articles/PMC12215417 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC12215417/) [↩](#cite-ref-4-1 "Back to text") 5. 5. [ pmc.ncbi.nlm.nih.gov/articles/PMC4996702 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC4996702/) [↩](#cite-ref-5-1 "Back to text") 6. 6. [ pmc.ncbi.nlm.nih.gov/articles/PMC8576512 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC8576512/) [↩](#cite-ref-6-1 "Back to text") 7. 7. [ pmc.ncbi.nlm.nih.gov/articles/PMC4823581 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC4823581/) [↩](#cite-ref-7-1 "Back to text") 8. 8. [ pmc.ncbi.nlm.nih.gov/articles/PMC8424989 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC8424989/) [↩](#cite-ref-8-1 "Back to text") 9. 9. [ pmc.ncbi.nlm.nih.gov/articles/PMC7121477 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC7121477/) [↩](#cite-ref-9-1 "Back to text") 10. 10. Practical compendium of antiarrhythmic drugs: a clinical consensus statement of the European Heart Rhythm Association of the European Society of Cardiology. Europace. 2025. PMCID: PMC12367031. 11. 11. The Atrioventricular Node Revisited. Arrhythmia & Electrophysiology Review. 2025. PMCID: PMC12215417. 12. 12. Diagnosis and Management of Complex Reentrant Arrhythmias Involving the His-Purkinje System. Arrhythmia & Electrophysiology Review. 2021. PMCID: PMC8576512. 13. 13. A comparative review on heart ion channels, action potentials and electrocardiogram in rodents and human: extrapolation of experimental insights to clinic. 2021. PMCID: PMC8424989. 14. 14. Mechanisms of cardiac arrhythmias. 2016. PMCID: PMC4823581. 15. 15. American Heart Association. Part 9: Adult Advanced Life Support. 2025 American Heart Association Guidelines for CPR and Emergency Cardiovascular Care. Study pathway Get faster at Emergency Medicine decision‑making -------------------------------------------------- - Rapid, exam‑style questions across core ED topics - High‑yield differentials and next‑step management - Target weak areas with smart review Free 5-day trial No credit card required. [ Start practicing ](https://mdster.com/user/dashboard) [ Explore Emergency Medicine ](https://mdster.com/speciality/emergency-medicine) [ View pricing ](https://mdster.com/pricing) [ Explore features ](https://mdster.com/features) No credit card required. 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