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Even if small amounts are ingested over long periods of time, the prolonged high levels of calcium ions have large negative effects on the animals. [30] The issues these animals experience are muscle weakness, and calcification of blood vessels, heart valves, liver, kidneys, and other soft tissues, which eventually can lead to death.
Though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line. [14] Onset of action is less than one to three minutes and lasts about 30–60 minutes. [14] The goal of treatment is to normalise the EKG and doses can be repeated if the EKG does not improve within a few minutes. [14]
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect (i.e. increased responsiveness) due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. [7]
[17] [18] The influx of calcium ions (Ca 2+) through L-type calcium channels also constitutes a minor part of the depolarisation effect. [19] The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dt max .
They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. [ 5 ] [ 6 ] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger.
The US Institute of Medicine (IOM) established Recommended Dietary Allowances (RDAs) for calcium in 1997 and updated those values in 2011. [6] See table. The European Food Safety Authority (EFSA) uses the term Population Reference Intake (PRIs) instead of RDAs and sets slightly different numbers: ages 4–10 800 mg, ages 11–17 1150 mg, ages 18–24 1000 mg, and >25 years 950 mg. [10]