Summary of material from Guyton and Hall (Chapters 9, 10, 11, 13, 21). This is about the conduction in and the contraction of the heart. There is also a short piece about heart arrhythmias. Three chapters are written in English, two chapters in Dutch.
Guyton and Hall, Medical Physiology
Chapter 9 – Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves
The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular
muscle and specialized excitatory and conductive muscle fibers. Duration of contraction of
atrial and ventricular muscle is much longer than skeletal muscle. The excitatory muscle
fibers does not really contract.
Cardiac muscle is striated and contains actin and myosin filaments. It also has intercalated
discs. At each intercalated disc the cell membranes fuse with one another to form permeable
gap junctions that allow rapid diffusion of ions. Thus, cardiac muscle is a syncytium of many
heart muscle cells (multinucleated cell that can result from multiple cell fusions).
Atrial syncytium walls of the two atria
Ventricular syncytium walls of the two ventricles
The action potential in ventricular muscle fiber rises to 20 mV. After the initial spike, the
membrane remains depolarized for about 0.2 s, exhibiting a plateau, followed at the end of
the plateau by abrupt repolarization.
In cardiac muscle, the action potential is caused by opening of two types of channels.
The L-type calcium channels are slower to open and remain open for several tenths
of a second, causing the plateau.
Immediately after the onset of the action potential, the permeability of cardiac
muscle membrane for potassium ions decreases about fivefold (this does not happen
in skeletal muscle). The decreased potassium permeability greatly decreases the
outflux of positively charged potassium ions during the action potential plateau and
thereby prevents early return to its resting level.
The phases of the action potential in cardiac muscle:
Phase 0 depolarization, fast sodium channels open
Phase 1 initial repolarization, fast sodium channels close
Phase 2 plateau, L-type calcium channels open and fast potassium channels close
Phase 3 rapid repolarization, L-type calcium channels close and slow potassium
channels open
Phase 4 resting membrane potential, -90 mV
Velocity of signal conduction in atrial and ventricular muscle fibers is 0.3 to 0.5 m/s. In
Purkinje fibers that is 4 m/s.
The normal refractory period of the ventricles is 0.25 to 0.30 s. The normal refractory period
of the atria is 0.15 s.
Excitation-contraction coupling is the mechanism by which the action potential causes the
myofibrils of muscle to contract. In cardiac muscle calcium ions also diffuse into the
sarcoplasm from the T tubules themselves at the time of an action potential, which opens
voltage-dependent calcium channels in the membrane of the T tubule. Calcium entering the
cell then activates calcium release channels (also ryanodine receptor channels). Then the
calcium ions interact with troponin to initiate contraction.
The strength of contraction of cardiac muscle depends to a great extent on the
concentration of calcium ions in the extracellular fluids.
The duration of cardiac muscle in the atria is about 0.2 s and in the ventricles about 0.3 s.
Diastole is a period of relaxation, heart fills with blood.
Systole is a period of contraction.
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