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Electrolyte Abnormalities. Dan Quan, DO Department of Emergency Medicine Maricopa Medical Center Phoenix, Arizona. Electrolyte Abnormalities That May Cause Life Threatening Conditions. Potassium Disorders Magnesium Disorders Sodium Disorders. Potassium.
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Electrolyte Abnormalities Dan Quan, DO Department of Emergency Medicine Maricopa Medical Center Phoenix, Arizona
Electrolyte Abnormalities That May Cause Life Threatening Conditions • Potassium Disorders • Magnesium Disorders • Sodium Disorders
Potassium • Most potassium regulation is done by the kidney (95%) • Most abundant intracellular cation
Hyperkalemia • Effects • Depolarizes the cell membrane • Slow ventricular conduction • Decreases action potential duration
Hyperkalemia Electrocardiogram • Normal sinus rhythm • Peaked T waves • Wide QRS • Loss of P waves • Sine wave, ventricular fibrillation, asystole • RBBB, LBBB, heart blocks Lack of EKG changes in the setting of hyperkalemia does not mean treatment should not be initiated
Hyperkalemia Immediate Treatment = IV Calcium • Peripheral IV: 1 ampule calcium gluconate (93 mg) • Central lines: 1 ampule calcium chloride (360 mg) • Stabilizes the excited myocardium by decreasing the resting membrane potential • Onset of action < 3 minutes, Duration of action 30-60 minutes, may repeat in 5 minutes if no effect seen • Infuse IV over 10 minutes • May be given empirically in most cases
HyperkalemiaPushin’ It Back (Into the cell) • IV glucose and insulin • Glucose is given to prevent hypoglycemia • 1 amp (25 g) dextrose 50% (D50) • Regular insulin 10 units IV push • Onset is 20 minutes, Duration of action 30-60 minutes • Albuterol nebulizer treatment • 20 mg over 10 min (decreases K+ by 1 mEq/L) • Onset is 30 minutes, Duration of action 2 hours • Albuterol MDI delivers 90 mcg per spray
HyperkalemiaHey, What About Sodium Bicarb? • Sodium bicarbonate in bolus doses does not decrease potassium in dialysis patients • Does not shift potassium back into the cell • Only after a 4 hour infusion did it decrease potassium by 0.6 mEq/L • May still be useful in those with a metabolic acidosis
HyperkalemiaGettin’ It Out • Furosemide 40–80 mg IV • Onset of action 15 minutes, Duration of action 2–3 hours • Sodium polystyrene sulfonate (Kayexalate) 15–30 g • Onset 2 hours, Duration of action 4–6 hours • No good evidence this does much • Hemodialysis • Onset immediate once it is initiated, Duration of action 3 hours • Removes about 1.5 mEq/L/hour
Hyperkalemia • Cardiac monitor or Serial EKGs for cardiac abnormalities • Lab draw after 1 to 2 hours after therapy initiated to assess treatment progress • May require further intervention
Hypokalemia • Most common causes of hypoK+ are: • GI losses • Diuretic use • Hypomagnesemia • Life threatening emergencies associated with hypoK+ • Diaphragmatic weakness, rhabdomyolysis, and cardiac dysrhythmias (highest risk is a rapid drop to 2.5 mEq/L)
Does Hypomagnesemia Contribute? • Magnesium is a “channel closer” in kidney cells • Acts on the Na+/K+ ATPase as a cofactor • Low magnesium “opens” the channel causing potassium loss through urinary excretion • Replacing potassium without replacing magnesium may be futile (refractory hypokalemia)
Potassium Oral Dosing • In general: 10 mEq KCl raises plasma K+ 0.1 mEq/L • Readily absorbed by the GI tract • Immediate release preparations liquid KCl • No evidence for > 50 mEq in a single dose • Do not use extended release KCl (K-Dur) if immediate results are required • Avoid giving > 20 mEq in a single dose (administer every 2 hours) • Increases risk of GI bleeding
Potassium Intravenous Dosing • Infuse potassium chloride at no more than 10 to 20 mEq/hour • Higher rates should be given through a central line • Rates > 80 mEq/hour are associated with dysrhythmias
Magnesium • Where is magnesium located in the body? • 53% bone • 27% muscle • 19% soft tissue • 0.5% RBCs • 0.3% serum • The only way we can assess magnesium levels • Kidney is involved in regulation
Hypomagnesemia • Cardiovascular • Seen as prolonged PR and QT intervals on EKG • Also can cause SVT, PAC, PVC, atrial abnormalities including atrial fibrillation, junctional rhythms, ventricular tachycardia and fibrillation, torsades de pointes
Hypomagnesemia • Consider treatment in these patients • Alcoholics • Asthmatics • Stroke patients • Cardiac patients • Dysrhymias, MI, CHF with dysrhymias • Pregnant patients (preeclampsia) • Hypocalcemia or Hypokalemia • Neurologic problems – vertigo, ataxia, tremor fasciculation, seizures
HypomagnesemiaReplacement • Magnesium sulfate • 1 g is equivalent to 8 mEq of elemental Mg2+ • Maximum infusion rate is 7 minutes/gram • Faster infusion rates cause ventricular dysrhythmias • Oral replacement: Do not exceed 40 mEq of elemental Mg2+ (diarrhea) • Magnesium oxide • 400 mg is equivalent to 20 mEq of elemental Mg2+ • Severe hypomagnesmia replace 48 mEq over 24 hrs
HypomagnesemiaSpecific Recommendations • Seizures or an acute dysrhythmia • 8 to 16 mEq Mg2+ (MgSO4 1-2 g) IV over 5 to 10 minutes • Torsades de pointes • Advanced Cardiac Life Support Guidelines • Loading dose of 16 mEq Mg2+ (MgSO4 2 g) IV over 15 minutes • Then 8 mEq/hour (MgSO4 2 g/hour) • Preeclampsia • 32 mEq (MgSO4 4 g) then 8 mEq/hour (MgSO4 2 g/hour)
Hypermagnesemia • Occurs in renal impaired patients or iatragenic administration • 3 to 4 mEq/L • Hypotension, flushing, nausea, mental status change, hyporeflexia • 5 to 6 mEq/L • QRS widening, QT and PR prolongation, conduction abnormalities • 8 to 10 mEq/L • Severe muscle weakness, respiratory depression, cardiac arrest
Hypermagnesemia Treatment • Calcium 100 to 200 mg over 5-10 minutes IV • e.g. 1 amp calcium gluconate minimum • May require bolus dosing or continuous infusion (2–4 mg/kg/hr)
Hyponatremia • Many causes of hyponatremia • [Na+] < 125 mEq/L are associated with neurologic problems • Cerebral edema • Increased intracranial pressure (encephalopathy) • Seizures
Hyponatremia Management • Rapid correction is dangerous • Acute hyponatremia • More symptomatic • Can tolerate rapid correction • Corrected 1 to 2 mEq/L/hour • Chronic hyponatremia • Correct at 0.5 mEq/L/hour • Risk of central pontine myelinolysis
Central Pontine Myelinolysis • Demyelinating process of the pons • Appears 1 to 6 days after treatment and beyond • May be irreversible • Causes locked-in syndrome • Complete paralysis except for eye control • Mind functions normally
Emergent Treatment of Hyponatremia3% (Hypertonic) Saline • Treatment for any hyponatremia induced neurologic process • 100 mL bolus • Repeat in 30 minutes if no improvement • Raises [Na+] by 2 to 4 mEq/L • Avoid hypertonic saline drips
Hypokalemia Treatment Summary • KCl 10 mEq raises K+ by 1 mEq/L • Avoid slow release oral potassium when immediate absorption is required • Limit to 20 mEq per dose every 2 hours • No IV bolus K+ infusions! • Replace magnesium with potassium even when magnesium is normal
Hypomagnesemia Treatment Summary • Serum levels may not reflect total magnesium body stores and deficiency • For seizures, Torsades de Pointes • 8 to 16 mEq Mg2+ (MgSO4 1-2 g) IV • Preeclampsia and eclampsia • 32 mEq Mg2+ (MgSO4 4 g) IV
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Hyponatremia Treatment Summary • Treat hyponatremia with severe neurologic symptoms with hypertonic saline (3%) • 100 mL IV over 10 minutes • Avoid rapid correction • Central pontine myelinolysis
References • Riccardi A, Tasso F, Corti L, Panariello M, Lerza R. The emergency physician and the prompt management of severe hyperkalemia. Intern Emerg Med. 2012 Jul 29. • Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51. • Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007 Oct;18(10):2649-52. • Mount DB, Zandi-Nejad K. Disorders of Potassium Balance. Brenner and Rector's The Kidney 9th ed. • Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. 2005 Jan-Feb;20(1):3-17. • http://www.globalrph.com/magnesium_supplements.htm accessed 8/28/12 • Rosen’s Emergency Medicine • Francis GS. Cardiac complications in the intensive care unit. Clin Chest Med. 1999 Jun;20(2):269-85. • Taal: Brenner and Rector's The Kidney, 9th ed.