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Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. [5] The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L ), while levels less than 2.1 mmol/L are defined as hypocalcemic.
The level of aggressiveness of treatment and choice of treatment may change depending on the severity of the disturbance. [3] If the levels of an electrolyte are too low, a common response to electrolyte imbalance may be to prescribe supplementation.
Specific electrocardiogram (ECG) changes may be seen. [1] Treatment is with magnesium either by mouth or intravenously. [2] For those with severe symptoms, intravenous magnesium sulfate may be used. [1] Associated low potassium or low calcium should also be treated. [2] The condition is relatively common among people in hospitals. [2]
Both early onset hypocalcemia (presents within 72h of birth) and late onset hypocalcemia (presents in 3-7 days after birth) require calcium supplementation treatment. Infants with intrauterine growth retardation, perinatal asphyxia, preterm, and diabetic mothers are most likely to develop neonatal hypocalcemia. [1]
Vitamin D related hypocalcemia may be associated with a lack of vitamin D in the diet, a lack of sufficient UV exposure, or disturbances in renal function. Low vitamin D in the body can lead to a lack of calcium absorption and secondary hyperparathyroidism (hypocalcemia and raised parathyroid hormone). [1]
Finally, though electrolytes can present variably, PCAS patients most often demonstrate hypokalemia, hypocalcemia and hypomagnesaemia [8] Acute kidney injury is not the leading cause of death after cardiac arrest. However, evidence suggests that the kidney damage after a cardiac arrest should be highly considered in the prognosis of the ...
Anticoagulants: To prevent embolization.. Beta blockers: To block the effects of certain hormones on the heart to slow the heart rate.. Calcium Channel Blockers: Help slow the heart rate by blocking the number of electrical impulses that pass through the AV node into the lower heart chambers (ventricles).
In addition, factors such as rapid infusion, concurrent use of more than one drug known to prolong QT interval, diuretic treatment, electrolyte derangements (hypokalemia, hypomagnesemia, or hypocalcemia), advanced age, bradyarrhythmias, and female sex have all been shown to be risk factors for developing drug-induced QT prolongation. [2]