Lec. 1. Rhythmicity of the heart.

Intro.

The properties of the heart include auto-rhythmicity, excitability, conductivity, and contractility.

Auto-rhythmicity.

Automaticity + Rhythmicity means that the heart can regularly and rhythmically self-excite. The mechanism is as follows:

Mechanisms of auto-rhythmicity.

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• The heart relies on self-generated myogenic impulses instead of the more typical neurogenic ones.
• These impulses are generated by the SA node AKA the “pacemaker” of the heart. (all parts of the heart are auto-rhythmic, for ex.: AV node is the 2ry pacemaker, Purkinje systems is the 3ry pacemaker, Cardiac muscle cells are the 4ry pacemaker.)

How is the pulse generated?

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1. Influx of Na⁺ through funny Na⁺ channels initiates depolarization from -60mv.
2. Influx of Ca⁺⁺ through T (Transient) Ca⁺⁺ channels continues depolarization.
3. Influx of Ca⁺⁺ through L (latent) Ca⁺⁺ channels further depolarizes the cell until threshold is reached.
4. Influx of Ca⁺⁺ continues through the L channels causing membrane potential to reach +10mv at which they become inactivated and close. At the same time, K⁺ channels open allowing K⁺ efflux and membrane potential starts to drop.
5. Influx of Na⁺ through funny Na⁺ channels which starts the next action potential.

Factors affecting rhythmicity.

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Cardiac innervation.

Can be summed up in:

• Sympathetic stimulation.
  • Causes tachycardia.
  • Decreases SA node permeability to K⁺ leading to less K⁺ being available for repolarization causing hyper-excitability of SA node (increased slope) and increased HR.
• Parasympathetic stimulation.
  • Causes bradycardia.
  • Increases SA node permeability to K⁺ leading to more K⁺ being available for repolarization causing hypo-excitability of SA node (decreased slope) and decreased HR.

Ionic concentrations.

Mostly regarding Na⁺ and K⁺ concentrations:

• K⁺ conc.:
  • Decreased K⁺ ⇒ Tachycardia.
  • Increased K⁺ ⇒ Bradycardia.
• Na⁺ conc.:
  • Decreased Na⁺ ⇒ inability to initiate impulse.
  • Increased Na⁺ ⇒ initiates impulse, but cant maintain it.

Physical factors.

• Cooling. ⇒ Bradycardia.
• Heating. ⇒ Tachycardia.
• Exercise. ⇒ Tachycardia.
• Endurance athletes. ⇒ Resting Bradycardia.

Chemical factors.

• Thyroid hormones & catecholamines. ⇒ Tachycardia.
• Acetylcholine. ⇒ Bradycardia.
• Hypoxia. ⇒ Bradycardia.

(Bradycardia = reduced rhythmicity. Tachycardia = increased rhythmicity.)

Electrical activity of contractile muscle fibers.

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Contractile cells demonstrate a much more stable resting phase than conductive cells at approximately −80 mV for cells in the atria and −90 mV for cells in the ventricles.

AP of contractile muscle fibers.

1. Na⁺ channels open allowing influx of Na⁺ ions, raising membrane potential to +30 mV.
2. At 30 mV, Na⁺ cannels close and K⁺ channels open allowing outflux of K⁺ ions.
3. Repolarization is slow due to opening of slow Ca⁺⁺ channels allowing slow influx of Ca⁺⁺ ==opposing the outflux of K⁺, causing a plateau==.
4. Once membrane potential reaches 0 mV Ca⁺⁺ channels close, causing rapid repolarization to RMP due to electrically unopposed K⁺ outflux.
5. ==Na-K pumps activate to restore Na⁺ and K⁺ concentration==.

(Phases start from 0, so number 1 is actually phase-0, number 2 is actually phase-1, and so on.)

Why is the plateau important?

• The plateau prolongs ARP of cardiac muscle which prevents Tetanization of the heart.
• The Ca⁺⁺ influx during the plateau provides 20% of the Ca⁺⁺ required for contraction.

Tetanization: Muscles contracting in place, not producing any tension, AKA spasm.

Overdrive suppression: The center with the highest BPM becomes the pacemaker of the heart. (due to the ARP in the plateau, the cardiac muscles will only respond to the fastest.)