Generally, calcium is administered to hyperkalemic patients to stabilize the cardiac myocytes by restoring their normal resting membrane potential (Fisch, 1973).
It is generally reserved for moderate to severely hyperkalemic patients with cardiac instability. Although there are no clear guidelines or evidence demonstrating the exact point to administer calcium, many clinicians will administer it if:
(1) the EKG shows evidence of cardiac destabilization such as widening QRS or loss of p-waves on EKG (be advised that EKG findings in patients with hyperkalemia can vary from patient to patient, and patients with severely elevated serum potassium levels may not manifest concomitant EKG findings);
(2) Serum potassium levels above 6.5-7mEq/L regardless of the presence of EKG changes
(3) rapid rises in serum potassium levels.
As a general rule, however, have a low threshold to administer calcium.
There are two options when administering calcium: calcium gluconate and calcium chloride.
Both types of calcium work relatively quickly in restabilizing the cardiac myocyte membrane, within 3-5 minutes.
Calcium chloride contains three times the concentration of calcium compared to calcium gluconate. Therefore, 1gm of calcium chloride is approximately equivalent to 3gm of Calcium gluconate.
Calcium chloride does not need metabolism by the liver in order to be bioavailable to cardiac myocytes, and thus is the preferred method of administration in patients with liver failure, cardiac arrest, or in shock states.
Calcium chloride, however, does pose a very serious risk for the development of tissue necrosis if it extravasates into the surrounding tissue (Semple, 1996). Therefore, it must be administered via a central venous line or a large bore, well-placed peripheral line.
Calcium gluconate, however, can be administered through a small peripheral IV if needed, as its risk of tissue necrosis is much less. Patients should be on a cardiac monitor when receiving calcium infusions.
It is generally reserved for moderate to severely hyperkalemic patients with cardiac instability. Although there are no clear guidelines or evidence demonstrating the exact point to administer calcium, many clinicians will administer it if:
(1) the EKG shows evidence of cardiac destabilization such as widening QRS or loss of p-waves on EKG (be advised that EKG findings in patients with hyperkalemia can vary from patient to patient, and patients with severely elevated serum potassium levels may not manifest concomitant EKG findings);
(2) Serum potassium levels above 6.5-7mEq/L regardless of the presence of EKG changes
(3) rapid rises in serum potassium levels.
As a general rule, however, have a low threshold to administer calcium.
There are two options when administering calcium: calcium gluconate and calcium chloride.
Both types of calcium work relatively quickly in restabilizing the cardiac myocyte membrane, within 3-5 minutes.
Calcium chloride contains three times the concentration of calcium compared to calcium gluconate. Therefore, 1gm of calcium chloride is approximately equivalent to 3gm of Calcium gluconate.
Calcium chloride does not need metabolism by the liver in order to be bioavailable to cardiac myocytes, and thus is the preferred method of administration in patients with liver failure, cardiac arrest, or in shock states.
Calcium chloride, however, does pose a very serious risk for the development of tissue necrosis if it extravasates into the surrounding tissue (Semple, 1996). Therefore, it must be administered via a central venous line or a large bore, well-placed peripheral line.
Calcium gluconate, however, can be administered through a small peripheral IV if needed, as its risk of tissue necrosis is much less. Patients should be on a cardiac monitor when receiving calcium infusions.
Circulation. 1973 Feb;47(2):408-19.
Anaesthesia. 1996 Jan;51(1):93
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