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To lower potassium, calcium chloride or calcium gluconate is preferred?

To lower potassium, calcium chloride or calcium gluconate is preferred?

The correct diagnosis and treatment of hyperkalemia has become a compulsory course and basic skill for clinicians.

In clinical practice, in the treatment of hyperkalemia, there are still some problems of one kind or another, especially some details of the problem, if not paid attention to, it may lead to delayed disease, and may even lead to serious consequences. Today, I would like to share with you 2 common clinical questions for your reference and study.

Calcium gluconate? calcium chloride?

The cardiotoxicity of anti-hyperkalemia with calcium is the first line of defense against hyperkalemia.

Commonly used calcium agents include calcium chloride and calcium gluconate injections. Both commonly use solutions at 10% concentrations, and due to the relatively high calcium content in calcium chloride molecules, 27.2 mg (0.68 mmol) of elemental calcium per 1 ml of 10% calcium chloride solution contains only 8.9 mg (0.22 mmol) of elemental calcium per 1 ml of solution (1).

It seems that calcium chloride solutions are more suitable for antagonizing cardiotoxicity of hyperkalemia due to their higher calcium ion content, but calcium chloride solutions in the intravenous infusion process, if extravased into the tissues will lead to tissue necrosis, therefore, the use of central veins as a pathway for infusion is generally recommended, which largely limits the use of calcium chloride.

Conversely, calcium gluconate solutions cause much less damage to blood vessels and peripheral tissues, and therefore can be treated with infusions through the peripheral vascular route. At the same time, combined with the domestic clinical practice, calcium gluconate solution seems to be more readily available than calcium chloride solution, so the most commonly used calcium agent in China is actually 10% grape calcium carbonate injection.

General usage is as follows: First, under close ECG monitoring, an intravenous bolus of 10% calcium gluconate injection of 10 mL is given for 2 to 3 minutes, and the ECG improvement effect should appear within 1 to 3 minutes and last for 30 to 60 minutes. If ineffective or relapsed, the dose may be repeated (2).

There is also a particular concern for the use of calcium: caution is required when combining with digitalis drugs, as hypercalcemia can exacerbate the toxic effects of digitalis on the myocardium (3).

In this case, if calcium must be used, 10 mL of 10% calcium gluconate injection should be added to 100 mL of 5% glucose injection in slow intravenous drips and dripped in 20 to 30 minutes to avoid the occurrence of hypercalcaemia and to enable even and slow distribution of calcium ions to the extracellular (4) (5).

The last precaution for the use of calcium is not to use it at the same time with solutions containing bicarbonate, such as sodium bicarbonate injection. The main reason for this is to avoid the deposition of calcium carbonate.

Be wary of "pseudo-hyperkalemia"

The so-called "pseudokalemia", as the name suggests, refers to the test report overestimation of the true blood potassium level, which is a kind of "false positive" test result.

The more common causes of pseudokalemia can be broadly divided into the following categories (6):

1. Due to muscle tension and tourniquet ligation, too long time and other reasons, local muscle cell potassium ions spill into the blood, resulting in the measured blood potassium level is higher than the true serum potassium concentration;

2. Thrombocytosis, leukemia, and polycythemia can cause pseudohalkalemia due to the release of intracellular potassium ions into the blood;

3. Acute symptoms of anxiety during venipuncture may lead to hyperventilation, which in turn leads to respiratory alkalosis, resulting in redistribution of potassium ions inside and outside the cell;

4. The anticoagulant component in some laboratory collection blood collection tubes is K+-EDTA, which can cause false blood potassium levels to rise.

Therefore, when the laboratory reports the "critical value" of hyperkalemia, the first thing that needs to be judged is: Is it really hyperkalemia? Although in most cases, the laboratory department will not make mistakes, but the string of "pseudokalemia" can not be forgotten, especially if the test report does not match the clinical manifestations.

In addition to reviewing the blood collection link, the most important method is to fully combine the clinical manifestations, whether the patient has the common myocardial and skeletal muscle manifestations of hyperkalemia, such as: bradycardia, weakened heart sounds, numbness in the limbs, fatigue, muscle soreness, quadriplegia, etc.

There is also a very simple way to distinguish is to do an ECG: a typical ECG in patients with hyperkalemia will have A shortened Q-T interval, T wave high tip and other manifestations, and even severe P-R interval prolongation or even P wave disappearance. These manifestations are essential to determine whether hyperkalemia is true or false.

Of course, because patients with end-stage renal disease have been chronically hyperkalemia for a long time, it is likely that the heart has developed a tolerance to hyperkalemia, and studies have shown that as CKD progresses, the risk of death from the same degree of hyperkalemia actually decreases (7). Therefore, for some patients with chronic hyperkalemia, the above differentiation may sometimes not always be effective.

Author: Zika

Edit: Yu Fang

"Clinical Medication" is reprinted with permission

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