Hyperkalemia medical therapy: Difference between revisions
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==Overview== | ==Overview== | ||
When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower potassium levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition. | When [[Cardiac arrhythmia|arrhythmias]] occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower potassium levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition. | ||
==Medical Therapy== | ==Medical Therapy== | ||
* [[Calcium]] supplementation (calcium gluconate 10%), preferably through a [[central venous catheter]] as the calcium may cause [[phlebitis]]) does not lower potassium but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]] <ref name="pmid25415806">{{cite journal| author=Ingelfinger JR| title=A new era for the treatment of hyperkalemia? | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 3 | pages= 275-7 | pmid=25415806 | doi=10.1056/NEJMe1414112 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25415806 }} </ref> | * [[Calcium]] supplementation (calcium gluconate 10%), preferably through a [[central venous catheter]] as the calcium may cause [[phlebitis]]) does not lower potassium but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]] <ref name="pmid25415806">{{cite journal| author=Ingelfinger JR| title=A new era for the treatment of hyperkalemia? | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 3 | pages= 275-7 | pmid=25415806 | doi=10.1056/NEJMe1414112 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25415806 }} </ref> | ||
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* [[Insulin]] will lead to a shift of potassium ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]]. | * [[Insulin]] will lead to a shift of potassium ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]]. | ||
* [[Bicarbonate]] therapy is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]]. | * [[Bicarbonate]] therapy is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]]. | ||
* [[Salbutamol]] (albuterol, Ventolin<sup>®</sup>) is a β<sub>2</sub>-selective | * [[Salbutamol]] (albuterol, Ventolin<sup>®</sup>) is a β<sub>2</sub>-selective [[catecholamine]] that his drug promotes movement of K<sup>+</sup> into cells, lowering the blood levels. | ||
* [[Polystyrene sulfonate]] (calcium resonium, kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation.[[enema|nem]][[defecation|ti]]. This medication may cause diarrhea and takes a lot of time to lower the potassium levels. | * [[Polystyrene sulfonate]] (calcium resonium, kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation.[[enema|nem]][[defecation|ti]]. This medication may cause diarrhea and takes a lot of time to lower the potassium levels. | ||
* Refractory or severe cases may need [[dialysis]] to remove the potassium from the circulation. | * Refractory or severe cases may need [[dialysis]] to remove the potassium from the circulation. |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Jogeet Singh Sekhon
Overview
When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower potassium levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.
Medical Therapy
- Calcium supplementation (calcium gluconate 10%), preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias [1]
- Magnesium sulfate is used to stabilize cardiac membrane in cases of hyperkalemia due to digoxin toxicity and hyperkalemia in hypercalcemic states.
- Insulin will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.
- Bicarbonate therapy is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase.
- Salbutamol (albuterol, Ventolin®) is a β2-selective catecholamine that his drug promotes movement of K+ into cells, lowering the blood levels.
- Polystyrene sulfonate (calcium resonium, kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation.nemti. This medication may cause diarrhea and takes a lot of time to lower the potassium levels.
- Refractory or severe cases may need dialysis to remove the potassium from the circulation.
- Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a diuretic (such as furosemide (Lasix®) or hydrochlorothiazide).
- Patiromer anion is a potassium binding ion cation exchange polymer that increases the gastrointestinal excretion of potassium. Patiromer should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.
Practical approach to treat hyperkalemia
- Rule out pseudohyperkalemia
- Look for ECG changes
- Look for reversible causes of hyperkalemia such as supplemental potassium
- Look for other causes such as acidosis or Diabetic ketoacidosis and treat accordingly.
1.Cardiac Membrane stabilization
- If ECG changes present or severe hyperkalemia
- Intravenous calcium gluconate 10% 0.5ml/kg loading dose.
2.Increase potassium shift from extracellular to intracellular spaces
- IV insulin with 2.5-5 ml/kg/h 20% dextrose (0.5-1 g/kg/h) with insulin 0.2 units for every gram of glucose administered.[2][3]
Salbutamol (ten drops of standard sabutamol inhalation solution contain 2.5 mg) | iv: 4-5 μg/kg in 15 ml of 5% dextrose/water, short infusion over 15 min |
Nebulized: 2.5 mg if <25 kg and 5 mg if >25 kg |
- Alternate regime-Bicarbonate(Sodium bicarbonate 8.4%) 1-2 mmol/kg over 30-60 min or calculated on base-deficit in cases of acidosis. [4]
3.Increase potassium excretion [5]
- Furosemide can be given Intravenously or orally, in dose of 1-2mg/kg.
- Polystyrene sulfonate (Calcium Resonium, Kayexalate) given P.O or P.r given in the dose of 1g\kg.
- Renal replacement therapy-It is the most effective manner to remove potassium.Haemodialysis is usually done in patients with severe hyperkalemia in chronic renal failure patients.[6]
Contraindicated medications
Hyperkalemia is considered a relative contraindication to the use of the following medications:
Hyperkalemia (Serum potassium >5.5 mEq/L) is considered an absolute contraindication to the use of the following medications:
References
- ↑ Ingelfinger JR (2015). "A new era for the treatment of hyperkalemia?". N Engl J Med. 372 (3): 275–7. doi:10.1056/NEJMe1414112. PMID 25415806.
- ↑ Alvestrand A, Wahren J, Smith D, DeFronzo RA (1984). "Insulin-mediated potassium uptake is normal in uremic and healthy subjects". Am J Physiol. 246 (2 Pt 1): E174–80. doi:10.1152/ajpendo.1984.246.2.E174. PMID 6364842.
- ↑ Blumberg A, Weidmann P, Shaw S, Gnädinger M (1988). "Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure". Am J Med. 85 (4): 507–12. PMID 3052050.
- ↑ Blumberg A, Weidmann P, Ferrari P (1992). "Effect of prolonged bicarbonate administration on plasma potassium in terminal renal failure". Kidney Int. 41 (2): 369–74. PMID 1552710.
- ↑ Allon M (1995). "Hyperkalemia in end-stage renal disease: mechanisms and management". J Am Soc Nephrol. 6 (4): 1134–42. PMID 8589279.
- ↑ Allon M, Shanklin N (1995). "Effect of albuterol treatment on subsequent dialytic potassium removal". Am J Kidney Dis. 26 (4): 607–13. PMID 7573015.