L10 CVS Physiology 4 Electrical properties of the heart

Overview

This lecture explains why the heart beats spontaneously and rhythmically, and how that beat is controlled and conducted. It covers the pacemaker (SA node) action potential and the ionic currents that generate it, how the autonomic nervous system speeds or slows the SA node, the anatomy and conduction velocities of the specialised conducting system that spreads excitation from atria to ventricles, the myocardium as an electrically coupled functional syncytium, the distinct five-phase ventricular myocyte action potential, and the long cardiac refractory period that prevents tetanic contraction.

The SA node pacemaker potential

The SA node is the heart’s dominant pacemaker because, unlike ordinary myocardial cells, its resting membrane potential (RMP) is unstable and depolarises spontaneously, rhythmically and at a rate that can vary. This instability arises because potassium permeability (PK) is lower in SA nodal cells than in myocardial cells, so the RMP sits less negative to begin with.

The SA node action potential has three phases, not five:

• Phase 4 (pre-potential / pacemaker potential): starts at about -60 mV to -70 mV and declines spontaneously (becomes less negative) toward threshold (~-40 mV). This slow decay is driven by three overlapping changes:
  • The “funny current” (if), a special inward Na+ current that progressively depolarises the cell.
  • A gradual fall in membrane K+ permeability, so the outward current iK progressively falls, letting if dominate increasingly.
  • At about -50 mV to -40 mV, voltage-operated Ca2+ channels begin to open, producing a small inward Ca2+ current (iCaT) that contributes to the final third of the pacemaker potential and triggers the action potential.
• Phase 0 (upstroke): slow-rising (unlike ordinary myocardium) because SA (and AV) node cells lack functional fast Na+ channels. The upstroke is due primarily to the slow inward Ca2+ current (iCa,L). Progressive depolarisation is opposed by the outward K+ current (iK) as K+ channels begin to open.
• Phase 3 (late repolarisation): driven by the outward K+ current (iK).

The transcript shows an uncaptioned pair of diagrams (a membrane-potential trace annotated "Na+ enters" / "Ca2+ enters" / "K+ exits" with a threshold line, alongside relative-permeability curves for PNa+(F), PCa2+(T), PCa2+(L), PK+) recurring four times (slides 13, 40, 46, 54) with no slide title, caption or bullet text identifying which cell type or phase it illustrates. It appears alongside SA-node-pacemaker-potential content (slide 13) and later within a "six pack" summary build sequence (slides 40, 46, 54), where two of those recurrences (46, 54) replace the expected cumulative bullet list seen on the surrounding build slides. Recorded as seen, not resolved.

Autonomic control of the SA node

Resting heart rate is about 60-70 beats/min, rising to as much as 180 beats/min in heavy exercise. Heart rate is set by the frequency of SA pacemaker action potentials; the SA node’s own natural (intrinsic) discharge rate is about 100-110/min, but autonomic input reduces the resting rate to about 70/min because parasympathetic tone dominates at rest (“vagal tone” / “vagal braking”).

• Sympathetic stimulation increases heart rate. Noradrenaline (NA), released from sympathetic nerve endings, binds β1-adrenergic receptors, raising intracellular cyclic AMP. Cyclic AMP directly increases if (the funny current), and also activates protein kinase A (PKA), which phosphorylates the Ca2+ channel (increasing iCa) and the K+ channel involved in repolarisation (increasing iK). The net effect is a steeper pacemaker-potential slope (faster rate) and, via the extra iK, a shortened action potential duration, which is needed because without it the normally long cardiac action potential would limit how fast the heart could beat.
• Parasympathetic stimulation decreases heart rate, via two mechanisms after acetylcholine (ACh) binds the muscarinic M2 receptor:
  • A fall in intracellular cAMP (opposing the sympathetic pathway), reducing if and iCa and so reducing the slope of the pacemaker potential.
  • Direct activation of an ACh-sensitive K+ channel (KACh), increasing K+ permeability and hyperpolarising the cell (RMP becomes more negative). Atropine blocks the M2 receptor and so this effect.
  • Together, a reduced slope and a hyperpolarised starting point mean the cell takes longer to reach threshold, slowing heart rate. Increased parasympathetic tone causes bradycardia; decreased parasympathetic tone / increased sympathetic tone causes tachycardia.

The pacemaker hierarchy and conduction system

The SA node is the dominant pacemaker; lower-order pacemakers exist in the AV node and conducting system but are normally suppressed by the SA node’s faster rate. Their intrinsic rates: AV node 40-50 bpm, Purkinje system 20-30 bpm. If the SA node fails, one of these can take over as an “escape” rhythm. (The transcript illustrates this clinically with images of an implanted artificial pacemaker: a pulse generator with pacing leads to the atria/ventricles, a chest photograph of an implant site, and a chest X-ray showing the device and lead, but gives no accompanying explanatory text.)

The excitation-conduction system consists of the SA node, the AV node, the bundle of His, the left and right bundle branches, and the Purkinje fibres. To reach the ventricles, the action potential must pass through the atrioventricular ring. Conduction velocities differ markedly by region and this difference is functionally important:

• Atria: ~0.5 m/s
• AV node: ~0.05 m/s (the slowest segment)
• Bundle of His and bundle branches: ~1.0 m/s
• Purkinje fibres: ~5.0 m/s (the fastest, described separately as “rapid” conduction; one slide describes the bundle of His, bundle branches and Purkinje system together as conducting at ~5.0 m/s, while the repeated summary table separates the bundle of His/bundle branches at ~1.0 m/s from Purkinje fibres at ~5.0 m/s, transcribed as given)
• Ventricular myocardium: ~0.5 m/s

The slow AV-nodal conduction produces a deliberate delay that allows the atria to fully depolarise and contract before the ventricles are depolarised. The rapid His-bundle-branch-Purkinje system then allows a fairly synchronous depolarisation and contraction of all regions of the ventricles; the rapidly conducting fibres of this system are modified myocardial cells called Purkinje fibres.

Slide 30 shows two unlabelled, uncaptioned black-and-white portrait photographs alongside the text describing the His-bundle/Purkinje conduction system. They are likely intended to depict the discoverers referenced by that system's names (His, Purkinje), but the slide does not name them, so this is recorded as seen rather than inferred.

Myocardium as a functional syncytium

Cardiac muscle cells (myocardium) are interwoven and may branch at either end. They are joined at their boundaries by intercalated discs, which contain gap junctions (alongside desmosomes, which provide mechanical linkage). Gap junctions permit direct cell-to-cell conduction of excitation, so the myocardial cells behave as a functional syncytium: a stimulus arising anywhere in the ventricle leads to complete contraction of both chambers, i.e. an all-or-none contraction.

The ventricular myocyte action potential

Ventricular muscle cell action potentials are subdivided into five phases (0-4), each with a distinct dominant ionic current:

• Phase 4 (resting membrane potential): set by the resting outward K+ current (iK).
• Phase 0 (upstroke): a stimulus (action potential) from an adjacent cell causes a rapid increase in Na+ permeability. At threshold (~-65 mV), voltage-sensitive fast Na+ channels open, increasing Na+ conductance about 100-fold; Na+ floods in and the cell depolarises rapidly (1-2 ms), overshooting to about +40 mV. The membrane potential does not reach ENa because outward K+ current is still flowing throughout.
• Phase 1 (early repolarisation): the overshoot is brief because the fast Na+ channels self-inactivate, decreasing Na+ permeability; within a couple of milliseconds an outward K+ current (ito) repolarises the membrane by a few mV.
• Phase 2 (plateau): a feature unique to cardiac muscle. Voltage-operated Ca2+ channels, which begin to activate at about -30 mV (i.e. during the rapid upstroke), produce a small but sustained inward Ca2+ current. This inward Ca2+ current almost balances the outward K+ current, holding the membrane potential nearly stable at 0 mV to -20 mV.
• Phase 3 (late repolarisation): as the plateau ends, Ca2+ channels inactivate and K+ permeability rises; the resulting outward K+ current (iK) repolarises the cell back toward resting potential.

Refractory periods and the absence of tetany

The electrical (action potential) and mechanical (developed tension) events of cardiac contraction overlap considerably in time. As a result, cardiac contractile force cannot summate and cardiac muscle cannot produce tetanic contractions.

• Absolute refractory period (ARP): from the upstroke, through the plateau, and until repolarisation reaches about -20 mV, cardiac myocytes are completely inexcitable and no new action potential can be generated. The ARP lasts about 250 ms of a roughly 300 ms action potential. The mechanism is that voltage-sensitive fast Na+ channels inactivate within about 2 ms of opening and remain unable to reopen until the membrane potential falls below about -20 mV.
• Relative refractory period (RRP): follows the ARP and lasts about 50 ms. During the RRP a sufficiently strong stimulus can elicit a curtailed action potential with reduced upstroke velocity and amplitude (reduced Na+ entry) and shortened duration (correspondingly diminished Ca2+ entry through voltage-sensitive channels).

Because the ARP is almost as long as the action potential itself, the heart cannot be re-excited until it has already substantially relaxed, protecting it from the sustained (tetanic) contraction that would prevent effective pumping.

Self-test

1. Explain why the SA node, rather than an ordinary myocardial cell, is able to depolarise spontaneously.
2. Describe the ionic basis of the phase 4 pacemaker potential in the SA node, naming the currents involved and the order in which they contribute.
3. Distinguish the phase 0 upstroke of the SA node action potential from the phase 0 upstroke of a ventricular myocyte, and explain the cellular basis of the difference.
4. Describe the intracellular signalling pathway by which sympathetic stimulation increases heart rate, from noradrenaline binding to the resulting change in the pacemaker potential.
5. Explain why sympathetic stimulation, via protein kinase A, also increases iK in the SA node, and what would happen to heart rate without this effect.
6. Describe the two distinct mechanisms by which parasympathetic stimulation slows the heart rate.
7. What is “vagal tone”, and what happens to heart rate if it decreases while sympathetic drive increases?
8. List the pacemaker hierarchy from fastest to slowest with each region’s approximate intrinsic rate, and explain why the SA node normally controls heart rate.
9. Trace the pathway an action potential takes from the SA node to the ventricular myocardium, naming each structure in order.
10. Give the approximate conduction velocities of the atria, AV node, bundle of His/bundle branches, Purkinje fibres and ventricular myocardium, and explain the functional significance of the AV-nodal delay.
11. Explain what makes the myocardium a “functional syncytium” and what this means for how a stimulus in the ventricle spreads.
12. Describe the five phases of the ventricular myocyte action potential and the dominant ionic current in each.
13. What is unique about phase 2 of the ventricular action potential, and what two currents balance to sustain it?
14. Distinguish the absolute refractory period from the relative refractory period in the ventricular myocyte, giving approximate durations and the mechanism underlying the absolute refractory period.
15. Explain why cardiac muscle cannot produce a tetanic contraction, linking the timing of the refractory period to the timing of developed tension.
16. Integrative: a patient develops increased vagal tone at rest. Trace the effect from the SA node membrane through to the change in overall heart rate, and contrast what would happen to the AV-nodal delay if sympathetic tone dominated instead.

Answers

Reveal answers

1. SA nodal cells have lower K+ permeability (PK) than ordinary myocardial cells, so their resting membrane potential is less negative and, critically, unstable: it declines spontaneously, rhythmically and at a rate that can vary, generating action potentials without need of an external trigger.
2. The phase 4 pacemaker potential declines from about -60/-70 mV toward threshold (~-40 mV) due to: (i) the funny current (if), an inward Na+ current that progressively depolarises the cell; (ii) a gradual fall in K+ permeability, so the outward iK progressively declines, letting if dominate increasingly; (iii) once the cell reaches about -50 to -40 mV, opening of voltage-operated Ca2+ channels producing a small inward Ca2+ current (iCaT) that contributes to the final third of the potential and triggers the action potential.
3. In the SA node, phase 0 is a slow-rising upstroke because SA (and AV) node cells lack functional fast Na+ channels; it is driven mainly by the slow inward Ca2+ current (iCa,L), opposed by outward iK. In a ventricular myocyte, phase 0 is a rapid upstroke driven by fast, voltage-sensitive Na+ channels opening at threshold (~-65 mV), increasing Na+ conductance about 100-fold and producing a rapid (1-2 ms) depolarisation overshooting to about +40 mV.
4. Noradrenaline binds β1-adrenergic receptors on the SA node, raising intracellular cAMP. cAMP directly increases the funny current (if), and it also activates protein kinase A (PKA), which phosphorylates the Ca2+ channel to increase iCa. The combined rise in if and iCa steepens the slope of the pacemaker potential, so threshold is reached sooner and heart rate increases.
5. PKA also phosphorylates the K+ channel involved in repolarisation, increasing the repolarising K+ current (iK) and shortening the action potential’s duration. Without this shortening effect, the normally long cardiac action potential would limit how fast the heart could beat, since a new action potential cannot start until the previous one (and its refractory period) has ended.
6. (i) ACh binds M2 muscarinic receptors, lowering intracellular cAMP (opposing the sympathetic pathway), which reduces if and iCa and so reduces the slope of the pacemaker potential. (ii) ACh binding M2 also directly activates an ACh-sensitive K+ channel (KACh), increasing K+ permeability and hyperpolarising the cell, so it starts further from threshold. Both slow the time to reach threshold and so slow heart rate.
7. Vagal tone is the resting dominance of parasympathetic (vagal) input on the SA node, which reduces the SA node’s natural intrinsic rate of ~100 bpm down to a resting rate of about 70 bpm (“vagal braking”). If vagal tone decreases while sympathetic tone increases, heart rate rises toward tachycardia.
8. SA node (dominant, intrinsic ~100-110/min) > AV node (~40-50 bpm) > Purkinje system (~20-30 bpm). The SA node controls heart rate because its intrinsically faster discharge rate suppresses the slower lower-order pacemakers; if it fails, a lower pacemaker can produce an “escape” rhythm at its own, slower, intrinsic rate.
9. SA node -> atrial muscle -> AV node -> bundle of His -> left and right bundle branches -> Purkinje fibres -> ventricular myocardium (the action potential must also pass through the atrioventricular ring to reach the ventricles).
10. Atria ~0.5 m/s; AV node ~0.05 m/s; bundle of His/bundle branches ~1.0 m/s; Purkinje fibres ~5.0 m/s; ventricular myocardium ~0.5 m/s. The very slow AV-nodal conduction creates a deliberate delay that allows the atria to fully depolarise and contract before the ventricles begin depolarising, preserving efficient sequential (atria-then-ventricles) pumping.
11. Myocardial cells are interwoven, may branch, and are joined at intercalated discs that contain gap junctions, which allow direct cell-to-cell electrical conduction. This electrically couples the cells into a functional syncytium, so a stimulus arising at any point in the ventricle leads to complete, all-or-none contraction of both ventricular chambers rather than a localised response.
12. Phase 4 (resting potential): dominant current iK. Phase 0 (upstroke): fast Na+ channels open, iNa dominates. Phase 1 (early repolarisation): fast Na+ channels inactivate, transient outward K+ current ito causes a small notch. Phase 2 (plateau): sustained inward Ca2+ current (iCa-L) nearly balances outward iK. Phase 3 (late repolarisation): Ca2+ channels inactivate, outward iK dominates and repolarises the cell.
13. The plateau (phase 2) is a sustained depolarisation unique to cardiac muscle. It is sustained because the small, sustained inward Ca2+ current (through voltage-operated channels activating around -30 mV) is almost sufficient to counterbalance the outward K+ current, holding the membrane potential nearly stable at 0 mV to -20 mV.
14. Absolute refractory period (ARP): lasts about 250 ms of a ~300 ms action potential, spanning the upstroke, plateau, and repolarisation down to about -20 mV; the cell is completely inexcitable because fast Na+ channels inactivate within about 2 ms and cannot reopen until the membrane falls below -20 mV. Relative refractory period (RRP): lasts about 50 ms after the ARP; a strong stimulus can elicit a curtailed action potential with reduced amplitude/upstroke velocity (reduced Na+ entry) and shortened duration (reduced Ca2+ entry).
15. The action potential and developed tension overlap considerably in time, and the ARP lasts almost as long as the action potential itself (about 250 of 300 ms), so the cell remains inexcitable through most of its contraction. This means a second contraction cannot be triggered before the first has substantially relaxed, so contractile force cannot summate and tetanic contraction cannot occur.
16. Increased vagal tone: ACh binds M2 receptors on the SA node, lowering cAMP (reducing if and iCa, flattening the pacemaker slope) and directly opening KACh channels (hyperpolarising the cell). Both effects lengthen the time to reach threshold, slowing the SA node’s discharge rate and so lowering overall heart rate (bradycardia). If sympathetic tone dominated instead, NA/β1/cAMP/PKA signalling would steepen the pacemaker slope and increase iCa and iK (increasing rate and shortening AP duration); conduction velocity through the AV node is not itself described in the transcript as autonomically modulated, so the AV-nodal delay’s response to autonomic tone is not covered in this lecture and is not stated here.