Part 4 · Chapter 4.2

Cardiac Muscle

Cardiac muscle is striated but behaves as a functional syncytium via gap junctions (connexin 43). Cardiomyocytes fire ~300 ms action potentials with a distinctive plateau phase, and pacemaker cells in the sino-atrial (SA) node spontaneously depolarise via the funny current I_f. This chapter covers the ventricular AP, pacemaker mechanism, and the Frank-Starling length-tension regulation.

1. Ventricular Action Potential

Five phases: (0) rapid upstroke via voltage-gated Na⁺ (Nav1.5); (1) early repolarisation via transient outward K⁺ (Ito); (2) plateau — L-type Ca²⁺ (Cav1.2) inward balances delayed-rectifier K⁺ outward; (3) repolarisation — rapid delayed rectifier IKr, slow IKs; (4) resting potential — inward-rectifier IK1. The plateau (~200 ms) is the defining cardiac feature: sustains contraction, prevents tetanus.

2. SA Pacemaker

SA node cells lack a stable resting potential. Phase 4 slow depolarisation (diastolic depolarisation) is driven by:

I_f: HCN4-mediated “funny current” activated by hyperpolarisation.
Decaying I_K after preceding AP.
T-type and L-type Ca²⁺ as threshold approaches.
“Ca²⁺ clock”: rhythmic SR Ca²⁺ release drives NCX depolarising current (Maltsev-Lakatta coupled-clock model).

Simulation: Cardiac APs

Python

script.py55 lines

import numpy as np, matplotlib
matplotlib.use('Agg')
import matplotlib.pyplot as plt

# Ventricular myocyte AP: 5 phases
t = np.linspace(0, 400, 1000)
V = np.full_like(t, -85.0)

# Phase 0: Na upstroke
m = t < 2
V[m] = -85 + 115 * (t[m]/2)
# Phase 1: early repolarization
m = (t >= 2) & (t < 10)
V[m] = 30 - 12 * (t[m] - 2)/8
# Phase 2: plateau
m = (t >= 10) & (t < 250)
V[m] = 15 - 10 * (t[m]-10)/240
# Phase 3: repolarization
m = (t >= 250) & (t < 320)
V[m] = 5 - 90 * (t[m]-250)/70
# Phase 4: rest
m = t >= 320
V[m] = -85

# Pacemaker If vs ventricular: no If, no phase 4 slope
t2 = np.linspace(0, 800, 1000)
V_sa = np.full_like(t2, -65.0)
for i in range(1, len(t2)):
    if V_sa[i-1] < -50 and V_sa[i-1] > -65: V_sa[i] = V_sa[i-1] + 0.02  # slow depol
    elif V_sa[i-1] >= -50 and V_sa[i-1] < 20: V_sa[i] = V_sa[i-1] + 0.5  # AP
    elif V_sa[i-1] >= 20 and V_sa[i-1] > -65: V_sa[i] = V_sa[i-1] - 0.3
    else: V_sa[i] = V_sa[i-1]

fig, (ax1, ax2) = plt.subplots(1, 2, figsize=(14, 5), facecolor='#0a0f1e')
for ax in (ax1, ax2):
    ax.set_facecolor('#111e2f'); ax.tick_params(colors='#bae6fd')
    for s in ax.spines.values(): s.set_color('#334155')
    ax.grid(True, color='#334155', alpha=0.3)

ax1.plot(t, V, color='#f87171', lw=2.4)
for x, lbl in [(1, '0'), (6, '1'), (130, '2'), (285, '3'), (360, '4')]:
    ax1.annotate(lbl, (x, 35), color='#fbbf24', fontweight='bold')
ax1.set_xlabel('Time (ms)', color='#bae6fd')
ax1.set_ylabel('Vm (mV)', color='#bae6fd')
ax1.set_title('Ventricular AP: phases 0-4', color='#67e8f9', fontweight='bold')

ax2.plot(t2, V_sa, color='#34d399', lw=2)
ax2.set_xlabel('Time (ms)', color='#bae6fd')
ax2.set_ylabel('Vm (mV)', color='#bae6fd')
ax2.set_title('SA node: pacemaker If slope', color='#67e8f9', fontweight='bold')

plt.tight_layout()
plt.savefig('output.png', dpi=120, bbox_inches='tight', facecolor='#0a0f1e')
print('Ventricular AP ~300 ms; plateau (Ca L-type) sustains contraction')
print('SA pacemaker: If (HCN4) + T-type Ca + K+ deactivation drive phase 4')

Click Run to execute the Python code

Code will be executed with Python 3 on the server

3. Frank-Starling Law

Cardiac muscle produces more force when stretched, up to an optimum. This Frank-Starling behaviour matches stroke volume to venous return beat-by-beat without neural intervention. Mechanism: at longer sarcomere lengths, (a) more optimal thick-thin overlap, (b) increased myofilament Ca²⁺ sensitivity via titin-mediated lattice spacing. The ascending limb of the curve is the normal operating range; beyond ~2.3 µm force declines.

4. Autonomic Modulation

Sympathetic β₁-adrenergic activation via cAMP/PKA increases I_fslope (positive chronotropy), ICaL (positive inotropy), and SERCA rate (positive lusitropy, faster relaxation). Parasympathetic M2 (vagal) activation via G_iopens IKACh K⁺ channels (negative chronotropy) and reduces ICaL. These opposing inputs tune heart rate and contractility in real time.

Key References

• DiFrancesco, D. (2010). “The role of the funny current in pacemaker activity.” Circ. Res., 106, 434–446.

• Bers, D. M. (2002). “Cardiac excitation-contraction coupling.” Nature, 415, 198–205.

• Lakatta, E. G. & Maltsev, V. A. (2010). “A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart’s pacemaker.” Circ. Res., 106, 659–673.

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