In this article, we are going to review the treatment of Hyperkalemia in great detail.
So what is the definition of hyperkalemia? There is no universal definition of hyperkalemia, but a serum K+ concentration of ≥ 5.5 mmol/L is widely described as a hyperkalemic condition.
Moreover, Hyperkalemia can be categorized into mild, moderate, or severe where mild is considered to be (5.5-5.9 mmol/L), followed by moderate (6.0-6.4 mmol/L) and severe (≥6.5 mmol/L).
Mechanisms of hyperkalemia
There are two major mechanisms of hyperkalemia:
- Increased potassium release from cells (e.g., this happens in conditions such as severe hyperglycemia, and rhabdomyolysis).
- Reduced potassium excretion in urine (this could be due to, e.g., hypoaldosteronism or low aldo state. We create this low aldo state this by giving the medications such as ACE inhibitors, ARBs, and Aldosterone antagonists. All of these medications have s/e of increasing potassium and lastly renal failure).
Treatment of Hyperkalemia – STEP 1
So how do you treat this condition? What are our treatment steps?
The first step in the tx of hyperkalemia is stabilizing the myocardium with IV calcium. I know You are thinking what is the use of giving calcium? see having high calcium levels is going to directly antagonizes the actions of hyperkalemia or high k+ levels on the Cardiac myocyte membrane. Whereas having low levels of calcium is going to increase the cardiotoxicity of hyperkalemia. So Calcium is not only helping your bones but also it strengthens or stabilizes your membrane from dangerous high potassium levels. It protects you from having cardiotoxicity and severe muscle weakness or paralysis.
differences between CALCIUM GLUCONATE AND CALCIUM CHLORIDE
- The 1st diff is – Calcium gluconate is given through the peripheral venous line whereas calcium chloride is given through the central venous line followed by
- The 2nd diff is – In terms of doses to be given, the usual dose of calcium gluconate is 1g (i.e., like 10 mL of a 10 percent solution). This is infused over two to three minutes, with constant cardiac monitoring. Whereas the usual dose of calcium chloride is 500mg to 1g (i.e. 5 to 10 mL of a 10 percent solution).
So Even though both are given at same doses, but they vary in terms of the amount of calcium that the same dose consists of. When compared with calcium gluconate, the concentration of elemental calcium is three-time more in the Calcium chloride. This is because gluconate is a heavier molecule than chloride. So if u take a 1g dose or 10ml of 10% solution of calcium gluconate most of the dose is wasted in accommodating the gluconate molecule. Due to that reason we have less calcium here whereas the same 1g dose or 10ml of 10 percent solution of calcium chloride has more calcium. This is due to the less molecular weight of chloride (13.6 versus 4.6 mEq in 10 mL of a 10 percent solution).
Out of these two, Calcium gluconate is generally preferred over calcium chloride due to 3 reasons
- Unlike concentrated calcium chloride infusions, calcium gluconate infusions do not cause any irritation at the injection site
- Calcium gluconate is safe, easy, and patient compliance to give via a peripheral venous line than central venous line.
- Generally, we reserve calcium chloride for the treatment of patients who are in cardiac arrest or who are near to cardiac arrest.
??? I want to ask you a question that should we give the IV calcium when there is hyperkalemia in digitalis toxicity patients. Because you know giving calcium in this condition can potentiate the cardiotoxicity.
The answer is “Yes” we can give. So When hyperkalemia occurs in digitalis toxicity patients, calcium can be administered even though hypercalcemia potentiates the cardiotoxic effects of digitalis. So unlike fast IV infusion to avoid acute hypercalcemia, here we slowly infuse a dilute 10 mL of 10 percent calcium gluconate solution in 100 mL of 5 percent dextrose in water over 20 to 30 minutes. Usually, In patients with hyperkalemia due to digitalis toxicity, the administration of digoxin-specific antibody fragments is the preferred therapy.
This is all about step-1 in the treatment of hyperkalemia
Treatment of Hyperkalemia – STEP 2
Here, In Step-2 we decrease the serum potassium.
This can be done in 3 ways:
- Stopping all exogenous sources of potassium
- Shifting the potassium into the cells
- Increasing the excretion of potassium
1. Stopping all exogenous sources of potassium
Stopping Intake of potassium from any possible exogenous sources of potassium like IV fluids, Enteral feeds, parenteral nutrition, dialysate, antibiotics, and blood products. This is one way by which we decrease the serum potassium.
2. Moving or shifting the potassium into the cells.
So here we shift the potassium from the serum into the cells such that our heart cannot see the presence of high potassium in serum and cannot react to it.
We do this either by 3 ways:
A. Giving Insulin with Glucose or
B. Giving beta-2 adrenergic agonists like Inhaled albuterol or
C. Giving intravenous Bicarbonate.
Let me elaborate on this
A. Giving Insulin with Glucose
- The exception to this rule is that we give insulin alone if the serum glucose concentration is >250mg/dl (i.e. 13.9mmol/l). Therefore, this indirectly refers to that we give only glucose if the serum concentration of glucose is <250mg/dl.
Commonly administered Insulin+Glucose
Regular insulin (10-20 units) in 500ml 0f 10% dextrose, IV, 60 min
B. Giving beta-2 adrenergic agonists like Inhaled albuterol
C. Giving intravenous Bicarbonate.
- Lastly, we can give bicarbonate and that will also help to shift the potassium into the cells. It does so via the mechanism of the potassium hydrogen exchange channels. Certainly, there is currently insufficient evidence to support the use of intravenous sodium bicarbonate for the acute treatment of hyperkalemia. So I don’t want to comment on this.
In a nutshell
In short, we’ve stabilized the cardiac membrane. We’ve stopped the intake of potassium and we have shifted the potassium into the cells. This is done either by giving Insulin with glucose, beta2 adrenergic agonists or sodium bicarbonate. Now let’s discuss the last way of decreasing the serum potassium. This can be done by increasing the excretion of potassium.
3. Increase the Excretion of potassium
You can increase the excretion of potassium by three methods like
- In method 1 we give k+ wasting diuretics like Loop diuretics for e.g furosemide to get rid of potassium through the urine
- In method 2 we give cation exchangers. For e.g Patiromer 8.4g orally can be given especially in patients with severe renal impairment in whom hemodialysis cannot be swiftly performed. Sodium polystyrene sulfonate (SPS) or Kayexalate 15 to 30g orally should not be given unless there are no other options to remove potassium from the body. Zirconium cyclosilicate is also given. All these drugs bind to potassium in the gastrointestinal tract in exchange for other cations, such as sodium or calcium.
There is one warning on Kayexalate or SPS from the FDA that it causes colonic necrosis. FDA has received 35 adverse event reports of serious bowel injuries (like bleeding, ischemic colitis, perforation). Many of them are fatal. The majority of these cases reported the concomitant use of sorbitol.
Furthermore, the 3rd method is like doing hemodialysis.
This is all about the treatment of hyperkalemia.
To some up In a nutshell first, we have stabilized the cardiac membrane by giving IV calcium gluconate. We’ve stopped the intake of potassium. We have shifted the potassium into the cells either by giving Insulin with glucose, beta2 adrenergic agonists or sodium bicarbonate. Lastly, we tried to excrete the potassium either by giving k+ wasting diuretics like Loop diuretics, cation exchangers and by hemodialysis.
CLINICAL FEATURES OF HYPERKALEMIA
Signs and symptoms are uncommon, and these tend to occur only when serum potassium is >7.0 mEq/L; For example, these include: muscle weakness, ventricular arrhythmias, Areflexia, Flaccid paralysis and Paresthesia (Decreased motor sensation)
- Tall peaked T waves.
- Shrinking and then the loss of P waves.
- Widening of the QRS interval and if we do not correct this, then it goes to “sine wave,” ventricular arrhythmia, and asystole.
Now in a clinical setting, when a patient comes to you, how do you apply all these?
Consider we had a patient here having abnormal potassium levels. So whenever there is an abnormal potassium level, first repeat the lab test. This is because the sample could be busted, or the cells could have hemolysed which might show high k+ levels earlier). If the lab tests come normal then there is no hyperkalemia. So consider this could be something else. If the lab tests are abnormal consider hyperkalemia.
So now once the hyperkalemia is confirmed, then do ECG or EKG. This is to say that the crucial evaluation of hyperkalemia is from ECG. However, In ECG everything gets changed as the K+ goes up. So at 5.5-6.5mEq/l, you see a peaked T wave. After that at 6.5-7.5 you see a loss of P waves. At 7.0-8.0 there is Widening of QRS, ultimately further widening of QRS leading to Sinewave at 8.0-10.0.`
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