2.2 The Cardiac Conduction System, Action Potentials & Ion Channel Physiology

2.2 The Cardiac Conduction System, Action Potentials & Ion Channel Physiology

Every number an RCES specialist measures — the AH interval, the effective refractory period, the sinus node recovery time, the response to adenosine — is a measurement of the physiology in this section. CCI's knowledge list names the cardiac conduction system, cardiac anatomy and physiology, cardiac pathophysiology, and normal intracardiac EGM and ECG interval values as testable areas.

---

1. The Conduction Hierarchy

Two properties of this table are constantly tested. The AV node is the slowest conducting tissue, and its delay is functional, not incidental: it produces the PR interval, allows atrial contribution to ventricular filling, and protects the ventricle from rapid atrial rates. The Purkinje system is the fastest, which is why a supraventricular impulse produces a narrow QRS while a ventricular focus, spreading muscle-to-muscle, produces a wide one.

The AV node and His bundle are the only normal electrical connection between atria and ventricles; the fibrous annuli insulate everything else. An accessory pathway is, by definition, a breach of that insulation.

---

2. The Fast-Response Action Potential

Atrial muscle, His-Purkinje tissue, and ventricular muscle share a five-phase action potential.

• Resting membrane potential is about −90 mV, maintained by IK1 and the Na⁺/K⁺ ATPase, which extrudes three sodium ions for every two potassium ions imported and is therefore electrogenic (net outward, hyperpolarizing).
• Phase 0 upstroke velocity (dV/dt) is 200-1,000 V/s, and it determines conduction velocity. Anything that reduces sodium current — class I antiarrhythmics, hyperkalemia, ischemic depolarization — slows conduction and widens the QRS.
• Phase 2 calcium entry triggers calcium-induced calcium release from the sarcoplasmic reticulum through the ryanodine receptor (RyR2), coupling excitation to contraction.

3. The Slow-Response Action Potential

Sinus node and AV nodal cells behave completely differently, and the difference explains most of EP pharmacology.

Because nodal cells rest near −55 mV, their fast sodium channels are permanently inactivated; they must use the slower calcium current. That single fact produces three consequences the exam tests relentlessly:

1. Decremental conduction. Recovery is time-dependent, so the earlier an impulse arrives, the longer it takes to conduct. This is why the AH interval lengthens as the A1-A2 coupling interval shortens, and why the AV node is the substrate for AV nodal reentry.
2. Calcium channel blockers and beta blockers work on the node, and adenosine hyperpolarizes it through IKACh — all three slow AV conduction while leaving His-Purkinje conduction untouched.
3. The HV interval does not prolong with faster pacing in a normal His-Purkinje system, because that tissue is fast-response and non-decremental. HV prolongation with pacing is pathologic.

Phase 4 automaticity and the funny current

Spontaneous phase 4 depolarization in pacemaker cells is driven by If, the "funny" current — an inward mixed sodium-potassium current carried by HCN channels, activated paradoxically by hyperpolarization and accelerated by intracellular cyclic AMP.

• Sympathetic stimulation (β₁ receptors → increased cAMP) steepens the phase 4 slope → faster rate.
• Vagal stimulation (M₂ receptors → decreased cAMP, plus IKACh-mediated hyperpolarization) flattens the slope and lowers maximum diastolic potential → slower rate.
• Ivabradine blocks If selectively, slowing the sinus rate without inotropic or AV nodal effects.
• Overdrive suppression: rapid pacing loads the cell with sodium, stimulating the electrogenic Na⁺/K⁺ ATPase, whose net outward current hyperpolarizes the cell and transiently suppresses automaticity. This is the mechanism measured by the sinus node recovery time.

---

4. Refractoriness

Refractoriness in fast-response tissue is voltage-dependent — it recovers as the membrane repolarizes, so it shortens at faster rates as the action potential duration shortens. Refractoriness in nodal tissue is time-dependent and lengthens with faster rates. That opposite behavior is the reason rapid atrial pacing produces AV Wenckebach rather than 1:1 conduction, and it is why an accessory pathway — which is fast-response, working-muscle-like tissue — conducts faster as atrial rate increases, making pre-excited atrial fibrillation lethal.

---

5. Autonomic Modulation

Vagal innervation is dense at the SA and AV nodes and sparse in the ventricle, which is why carotid sinus massage and the Valsalva maneuver terminate AV-nodal-dependent tachycardias but do nothing to ventricular tachycardia.

---

6. Arrhythmia Mechanisms

The exam expects clean separation of three mechanisms.

1. Abnormal automaticity. A focus depolarizes spontaneously and faster than the sinus node. It warms up and cools down, cannot be initiated or terminated by programmed stimulation, and is often catecholamine-sensitive. Examples: sinus tachycardia, some focal atrial tachycardias, accelerated idioventricular rhythm.

2. Triggered activity. Afterdepolarizations reach threshold and generate a new action potential. Two forms:

3. Reentry. By far the most common mechanism and the basis of nearly every ablated arrhythmia. Reentry requires three conditions simultaneously:

1. Two anatomically or functionally distinct pathways forming a circuit.
2. Unidirectional block in one limb.
3. Slow conduction in the other limb, long enough that the blocked limb recovers excitability before the wavefront returns.

        Premature beat
              |
              v
        [ Common proximal pathway ]
           /                \
   Fast pathway          Slow pathway
   (BLOCKED - long ERP)   (conducts slowly)
           ^                  |
           |                  v
           +---- retrograde <-+   ==> sustained reentry

Reentrant arrhythmias are reproducibly initiated and terminated by programmed stimulation, can be entrained, and have a fixed excitable gap — the three features exploited in every diagnostic pacing maneuver. AVNRT, AVRT, typical atrial flutter, and post-infarction ventricular tachycardia are all reentrant.