Cardiac muscle cannot be tetanised because of its very long refractory period, which is tied directly to the long duration of its action potential (the plateau).
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A skeletal muscle fiber has a brief action potential (a few milliseconds) and a very short refractory period. If stimuli arrive fast enough, a new contraction can be triggered before the previous one relaxes, causing summation and eventually a smooth, sustained contraction (tetanus).
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Cardiac muscle fibers, in contrast, have a long action potential with a plateau phase (phase 2), caused by sustained calcium influx through voltage-gated Ca2+ channels balanced against reduced K+ efflux. This plateau keeps the membrane depolarized for roughly 200-300 ms.
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During phases 0 through 2, and about half of phase 3 (until the membrane repolarizes to about -50 mV), the cardiac cell is in its absolute refractory period - no stimulus, however strong, can generate a new action potential. This is followed by a short relative refractory period until phase 4, during which only a very strong stimulus could re-excite the tissue.
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Because the refractory period (about 0.25-0.30 sec in the ventricle) lasts almost as long as the mechanical contraction itself, a second action potential (and thus a second contraction) cannot be initiated until the muscle has already begun to relax. This prevents wave summation, so premature stimuli produce isolated extra beats rather than a fused, tetanic contraction.
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Guyton and Hall Textbook of Medical Physiology, "Refractory Period of Cardiac Muscle"
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Ganong's Review of Medical Physiology, 26th Ed., "Resting Membrane & Action Potentials"
This is not incidental - it is essential for survival. The heart must relax between beats to allow ventricular filling and to pump blood rhythmically. As Ganong's puts it, "tetanization of cardiac muscle for any length of time would have lethal consequences," since a heart locked in sustained (tetanic) contraction could not fill with blood or eject it, and circulation would stop.