Critical Care Medicine
K, and Mg imbalance
- 1. Description of the problem
- 2. Emergency Management
Special considerations for nursing and allied health professionals.
Potassium and magnesium imbalance
Hyperkalemia, hypokalemia, hypermagnesemia, hypomagnesemia
Acidosis, alkalosis, malnutrition, malabsorption, diarrhea, chronic kidney disease (CKD), acute kidney injury (AKI), cardiac arrhythmia, diuretic effects
1. Description of the problem
Disorders of potassium: overview
Potassium (K) is an essential intracellular cation. 98% of total body K is intracellular; it is a main determinant of intracellular osmolality, and its transmembrane gradient regulates cell membrane resting electrical potential.
Intracellular concentration of K (100-150 mEq/L) is maintained via an active Na/K ATPase membrane active transport system that extrudes 3 Na ions from the cell and transports 2 K ions intracellularly against a steep K concentration gradient. Intracellular K diffuses passively across cell membranes; the magnitude of K transmembrane diffusion determines transmembrane electrical potential.
Intracellular entry of K is related to insulin-dependent intracellular transport of glucose and transmembrane H+ gradients. In metabolic acidosis, about 60% of H+ ions are buffered intracellularly and K exits the cell in exchange for H+. As a rule of thumb, for each 0.1 decrease in plasma pH, plasma K increases by about 0.6 (0.2-1.7) mEq/L.
Organic acidosis such as lactic and ketoacidosis are associated with lesser degrees of hyperkalemia than mineral acidosis. In metabolic alkalosis, K shifts intracellularly in exchange for H+. Hyperosmolality may cause extracellular K shifts, such as in severe hyperglycemia and after rapid intravenous administration of sodium bicarbonate. Plasma K concentration may rise as much as 0.4-0.8 mEq/L for every 10 mOsm/Kg increase in effective plasma osmolality.
Extracellular concentration of K (3.5-5.0 mEq/L) is small and tightly regulated. Abnormalities in extracellular K concentration may result in severe cardiac arrhythmias and skeletal muscle dysfunction.
Na/K ATPase is stimulated by catecholamines and insulin and its function is also dependent on thyroid hormones. Cathecholamines inhibitintracellular entry of K via α-receptors and stimulateintracellular entry of K via β2-receptor stimulation of Na/K ATPase. Insulin stimulates Na/K ATPase and promotes intracellular K entry. The primary physiologic effect of insulin and catecholamines is to facilitate the disposition of a K load. The ability to handle a K load is impaired in insulin deficiency.
Aldosterone promotes intracellular K entry and promotes renal and intestinal excretion of K.
Thyroid hormones, glucocorticoids and growth hormones maintain long-acting stimulation of Na/K ATPase.
Exercise: K is normally released from muscle cells during exercise in proportion to the intensity of exercise. Normally, the elevation in K level is transient and mild, but may be exacerbated to dangerous levels in patients on β-blockers.
The two pathways of excretion of K are intestinal and renal. Renal K excretion is tightly regulated to maintain balance between intake and output and stable K body contents. Intake and output is usually around 1.5 mEq/Kg/day. Renal K excretion is primarily stimulated by three factors: (1) increase in serum K concentration; (2) increase in serum aldosterone concentration (aldosterone increases the number of open apical cell sodium channels; increased Na reabsorption increases the electronegativity of the lumen and therefore enhances K secretion); and (3) enhanced delivery of sodium and water to the distal secretory site.
A K load is usually excreted in the urine in 6-8 hours in patients with normal renal function. Virtually all the K excreted in the urine is K secreted in the renal tubules; virtually all filtered K is reabsorbed completely in the proximal tubule and thick ascending loop of Henle (TALH). Renal excretion of K is regulated by modifying K tubular secretion. Renal tubular handling of K is closely associated with renal control of acid-base equilibrium and is tightly regulated by the renin-angiotensin-aldosterone axis
For more information, see chapter on "Disorders of Potassium, Magnesium and Calcium Balance."
Key points in disturbances of K balance
Body K stores can become abnormal either due to abnormal intake or abnormal losses, primarily renal or intestinal. Serum K can become abnormal due to abnormal body K stores or abnormal transmembrane distribution of K (K shifts).
Decreased K intake can lead to total body depletion of K and hypokalemia, which is defined as plasma K less than 3.5 mEq/L. Hypokalemia can lead to cardiac arrhythmia, especially among persons treated with digitalis.
Administration of diuretics is a common cause of K depletion and hypokalemia.
Metabolic alkalosis shifts K intracellularly in exchange for H+ exit from cells.
Severe vomiting can lead to hypokalemia and metabolic alkalosis; in this case, the main source of K loss is not in the vomit but in the urine, as a result of the metabolic alkalosis, secondary hyperaldosteronism and - in later stages of prolonged vomiting - urinary potassium bicarbonate excretion.
Primary and secondary hyperaldosteronism are associated with hypokalemia and metabolic alkalosis.
Excessive diarrheal loss of K can lead to hypokalemia and hyperchloremic metabolic acidosis due to intestinal loss of bicarbonate.
Rare congenital abnormalities such as Bartter's syndrome and Gitelman's syndrome induce metabolic alkalosis and hypokalemia.
Hyperkalemia is rare in subjects with normal renal function. As renal dysfunction progresses, the risk of hyperkalemia increases because the kidneys lose the ability to adjust the magnitude of K tubular secretion to the needs of body balance.
Hypercatabolic situations such as sepsis and high fever are frequently associated with hyperkalemia. In addition, intraintestinal erythrocyte breakdown in situations of gastrointestinal bleed frequently leads to hyperkalemia due to sudden body load of K due to intestinal absorption, while obstructive uropathies lead to disproportionate degrees of hyperkalemia primarily due to renal medullary injury and decreased prostaglandin medullary production.
Drugs are a main mechanism of hyperkalemia. Non-steroidal antinflammatory drugs may cause hyperkalemia either because they induce gastritis and GI bleed or because they decrease renal function and block intrarenal prostaglandin synthesis. Angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs) induce hypoaldosteronism and decreased tubular K secretion. Distal tubular secretion of K can be blocked by K-sparing diuretics such as amiloride and triamtirene, which block apical cell ENaC channels.
Trimetoprim (a component of the combination chemotherapeutic agent trimetoprim/sulfametoxazole) has similar effects to those of triamtirene and blocks K secretion, thus increasing the risk of hyperkalemia. Aldosterone-receptor competitive inhibitors such as spironolactone decrease renal K excretion.
Other conditions associated with hyperkalemia include:
Massive muscle breakdown such as in crush syndrome can be associated with life-threatening hyperkalemia: for each kilogram of crushed muscle, between 100-150 mEq of K can be released into the extracellular fluid.
For more information on hypokalemia, see "Hypokalemia" section above.
For more information on acid-base disorders, see , chapters on "Acid-Base Imbalance, Abnormal Blood Ph" and "Disorders of Potassium, Magnesium and Calcium Balance."
Disorders of magnesium: overview
Mg is a divalent cation atomic weight 24 which serves as an important cofactor to numerous enzymes, especially those involving ATP.
Mg homeostasis is largely controlled by the kidney.
Serum magnesium concentration may not reflect status of total body Mg.
During Mg depletion, the urinary fractional excretion (FEMg) is less than 2%.
Magnesium metabolism disturbances are associated with important consequences on membrane stability, hormone secretion, and neuromuscular and cardiovascular function.
Distribution of body magnesium
66% in skeleton, 33% intracellular (muscle and liver), 1% extracellular.
Serum Mg: normal range 1.6-2.4 mg/dl (1.4-2 mEq/L, or 0.7-1.0 mMol/L):
Ionized portion physiologically active moiety: 55-70% of total serum Mg.
Protein bound 20-30%, complexed 10-20%.
Total serum Mg levels correlate well with clinical manifestations quite independently of serum albumin levels.
Tissue Mg: 1/3 on the surface of hydroxyapatite crystals, 2/3 intracellularly within organelles, especially mitochondria. Control of intracellular Mg is poorly understood.
Normal Mg ingestion is about 300 mg/day, digestive secretions 30 mg, net absorption 30%, about 100 mg, usually balanced by similar urinary excretion.
Mg absorption not regulated; balance is maintained by renal excretion.
Magnesium depletion is unusual unless in patients with severe malnutrition. It is a common problem in severe alcoholics.
Majority of absorption in the ileum.
Non saturable component quantitatively the most important.
Role of vitamin D in Mg transport is controversial.
Phosphate binders limit Mg absorption.
Urinary excretion is the net result of glomerular filtration and tubular resorption.
Mg balance is achieved by changes in Mg resorption.
Mg filterable 80% (2000 mg/day), about 100 mg/day are excreted in the urine (1-3%).
During Mg depletion urinary excretion can decrease to less than 0.5% filtered load.
Proximal tubule reabsorbs 10-15% filtered load.
Thick ascending loop of Henle is responsible for about 70% tubular reabsorption: driven by transepithelial lumen positive electrical gradient generated by K recycling; in the thick ascending loop of Henle and distal tubule, the calcium sensor receptor CaSR regulates Ca and Mg reabsorption.
Distal tubule reabsorption (10%) is active and regulates Mg excretion; driven by electrical gradient, Mg enters the cell via the divalen ion channel TRPM6.
Regulation of magnesium metabolism: the important divalent sensing receptor CaSR responds to changes in plasma magnesium and calcium concentrations with a decrease in paracellular transport by affecting paracellin-1; this is the most important mechanism by which hypomagnesemia stimulates Mg conservation.
For more information, see Chapter on "Disorders of Potassium, Magnesium and Calcium Balance."
Symptoms of hypokalemia
Subjective: palpitations, muscle cramps, paralysis, constipation, nausea or vomiting, polyuria, nocturia, mental status changes; clinical manifestations uncommon unless serum K is less than 3 mEq/L, generally earlier and more severe if hypokalemia is acute.
Life-threatening: rhabdomyolysis and diaphragmatic weakness; cardiac arrhythmia (EKG changes: T wave flattening, inverted T wave, prominent U wave, ST segment depression, atrial or ventricular arrhythmia); epinephrine released during a stress response such as acute coronary ischemia drives K intracellularly and may increase the risk of ventricular arrhythmia.
Impaired urinary concentration and polyuria due to decreased tubular vasopressin responsiveness.
Increased renal ammonia production and increased net acid secretion causing metabolic alkalosis.
Inability to eliminate an Na load and fluid retention.
Chronic: hypokalemic nephropathy with interstitial fibrosis and tubular atrophy.
Symptoms of hyperkalemia
Clinical manifestations are due to change in the impaired neuromuscular transmission and altered membrane electrical potential; hyperkalemia initially determines hyperexcitability of plasma membrane but persistent depolarization inactivates sodium channels and leads to late decrease in membrane excitability.
Muscle weakness or paralysis.
EKG changes: Tall peaked T wave earliest change, followed by shortened QT interval. At higher K levels, there is progressive lengthening of the PR interval and QRS duration. Progressively P waves disappear and ultimately the QRS widens to form a sine wave, leading to ventricular arrest with flat EKG line.
Conduction abnormalities include right and left bundle branch and bifascicular block, and advanced atrioventricular block. Cardiac arrhythmias include sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, and fibrillation and ventricular asystole.
Progression and severity of EKG changes do not correlate with serum K concentration.
Clinical manifestations occur most frequently at serum levels greater than 7 mEq/L with chronic hyperkalemia or at lower levels in acute hyperkalemia.
Hyperkalemia may cause metabolic acidosis such as in renal tubular acidosis Type IV, where hyperkalemia inhibits renal ammonium (NH4) excretion.
Symptoms of hypomagnesemia
Hypomagnesemia is a very common and important condition, generally underestimated by serum Mg levels and caused by decreased intestinal absorption and decreased renal tubular reabsorption causing urinary loss. Hypomagnesia is defined as Mg levels less than 1.6 mg/dl (1.4 mEq/L or 0.7 mM). The characterization of the status of total Mg body stores is difficult. Symptoms include neuromascular effects, cardiac effects and disturbances in Ca and K homeostasis, which are very tightly associated to Mg depletion.
Trousseau's sign: sphyngomanometer cuff at 20 mmHg above systolic blood pressure causes carpal spasm.
Chvostek's sign: preauricular tapping of facial nerve causes twitching of nasolabial fold and lip, lateral eye angle and homolateral facial muscles.
Vertigo, chorea, ataxia, psychiatric changes.
Conduction disturbances, including the following EKG changes:
Prolonged PR and QT intervals.
Widening of the QRS complex.
Abnormal T and U waves.
Atrial and ventricular arrhythmia including Torsade des Pointes.
Exacerbation of digoxin toxicity.
Role in myocardial infarction
Concurrent electrolyte disturbances
Hypocalcemia: seen with severe hypomagnesemia less than 1.1 mg/dl; associated with hypoparathyroidism due to Mg depletion resulting from decreased PTH secretion and decreased response to PTH.
Closely interrelated phenomena.
Symptoms of hypermagnesemia
Clinically significant hypermagnesemia is uncommon in the presence of normal renal function and is almost always the result of either decreased renal function or increased enteral or parenteral Mg load. It is defined as serum Mg less than 2.4 mg/dl (2 mEq/L or 1 mM).
Clinical presentation of hypermagnesemia is related to the degree of hypermagnesemia, usually not evident until Mg levels are higher than 3-5 mg/dl. Symptoms of hypermagnesemia include:
Nausea and vomiting.
When serum mg levels are between 5-10 mg/dl, symptoms include:
EKG changes: prolongation PR, QRS and QT intervals.
Decreased deep tendon reflexes.
Severe hypermagnesemia (serum Mg greater than 10 mg/dl) can cause hypocalcemia by suppressing PTH secretion, which may result in:
Complete heart block.
2. Emergency Management
Cl2 (three times the Ca concentration in Cagluconate; must be administered via central line), or Ca gluconate (maybe administered via peripheral IV line).
Diagnose and correct underlying cause:
Always measure and replace Mg if low to facilitate treatment: hypomagnesemic patients can be resistant to correction of hypokalemia and have malignant arrhythmias such as Torsade des Pointes in patients susceptible such as those with prolonged QT interval.
Prevent life-threatening conditions:
Rapid drop K to less than 2.5 mEq/L and/or cardiac arrhythmias call for urgent replacement.
Replete K deficit:
Rule of thumb: in the absence of redistribution, K drops about 0.27 mEq/L for every 100 mEq K loss.
In chronic hypokalemia, a K deficit of 200-400 mEq is required to lower serum K by 1 mEq/L but those are only gross estimates: close monitoring is essential.
Supplementation recommended for K less than 3 mEq/L.
Potassium chloride is the preferred preparation because it simultaneously replenishes chloride lost in vomiting or diuretic effects. Chloride deficiency maintains and worsens concurrent metabolic alkalosis.
Enrich K in diet. K in foodstuffs is only 40% retained.
Prescribe KCl or K phosphate if hypophosphatemia present.
Cl repletion important to concurrently correct hypochloremic metabolic alkalosis if present.
Usual dose 20-80 mEq/day in divided 2-4 doses in mild to moderate hypokalemia (3.0-3.4 mEq/L).
Monitor K levels, which will fall back within a few hours due to intracellular redistribution.
Indicated in severe hypokalemia (<3.4 mEq/L) or symptomatic (such as arrhythmia or rhabdomyolysis).
Limited to patients unable to use enteral route or patient with severe signs or symptoms.
Administer in saline solution rather than dextrose as dextrose will enhance intracellular entry of K.
Usual infusion rate is 10 mEq/hour, maximum rate 10-20 mEq/hour in life-threatening situations, under continuous clinical and EKG monitoring to minimize risk of arrhythmia and respiratory depression, and paralysis.
Address concurrent causes such as diuretic effects and high Na intake.
Aggressive K repletion is usually limited to situations with severe K depletion such as diabetic ketoacidosis or hyperosmolar non-ketotic hyperglycemia, where patients have substantial urinary losses of K. In these situations, postpone initiation of insulin therapy until serum K exceeds 3-3.5 mEq/L.
Hyperkalemia may occur in the context of excess total body K, such as in patients with renal failure, excess K administration or effects of ACE inhibitors. In those cases, removal of excess K is the main goal of treatment.
Hyperkalemia may occur due to redistribution in patients with normal total body K stores such as in hyperkalemic periodic paralysis.
Hyperkalemia may occur in patients with depleted total K stores due to diabetic ketoacidosis or hyperosmolar hyperglycemia. In those cases, hyperkalemia may be followed by severe hypokalemia requiring K replacement.
Avoid fasting, especially in patients with end-stage renal disease, because low insulin levels may promote hyperkalemia. Non diabetic dialysis patients awaiting surgery should receive IV fluids containing glucose, and diabetic dialysis patients should receive a combination of glucose and low-dose insulin.
Address reversible causes:
Relieve urinary obstruction.
Discontinue NSAIDs and inhibitors of the renin-aldosterone system.
Emergency treatment if:
Symptomatic hyperkalemia, muscle weakness, paralysis.
K level exceeds 6 mEq/L.
Three components to treatment:
Antagonism of membrane effects of potassium:
Antagonizes membrane depolarization induced by hyperkalemia.
Indicated when EKG shows widened QRS or loss of P waves but no peaked T waves alone.
Begins immediately but is short lived.
Ca can be administered as CaCl2 (three times the Ca concentration in Ca gluconate; must be administered via central line), or Ca gluconate (may be administered via peripheral IV line).
Infuse IV over 2-3 minutes under constant EKG monitorning; can be repeated if EKG changes persist after 5 minutes.
Intracellular shift of potassium:
Insulin and glucose:
Induces K decrease of 0.5-1.5 mEq/L; begins to act in about 15 minutes and peaks at 60 minutes, wears off in 1-3 hours.
Use is controversial.
Effectiveness is uncertain, may actually induce further shift of K into the extracellular space.
Drive K intracellularly by stimulating Na/K ATPase.
Peak effect within 30-90 minutes with nebulization.
Removal of excess potassium
Loop diuretics more powerful and rapidly effective than thiazide diuretics.
Modest effect on K levels in the acute setting, especially in patients with CKD.
Sodium polystyrene sulfonate (SPS):
Can be used orally or - less effectively - as retention enema.
Dose usually 1 g/Kg/dose in children and 15-30 g in adults; may be repeated every 4-6 hours.
Effect may take 4-24 hours.
Effectiveness is controversial, especially among patients with end stage renal disease.
Ischemic colitis and colonic mucosal necrosis important complications attributed to SPS use or concomitant administration of high concentration sorbitol as a laxative.
Necrosis commoner when sorbitol used in high concentration (70%) but also reported when a 33% sorbitol concentration was used.
Use of the resin without sorbitolis preferable to decrease risk of intestinal necrosis.
FDA released a recommendation in 2009 that sodium polystyrene sulphonate should be used without sorbitol.
SPS plus sorbitol should not be used perioperatively as it further increases the risk of intestinal mucosal ischemia.
Avoid repeated/chronic use; address the reason for persistent hyperkalemia.
When the alternatives are SPS and dialysis, dialysis should be preferred if the patient already is on dialysis or in patients with severe degree of hyperkalemia and renal dysfunction who are unlikely to rapidly respond to conservative measures:
Intermittent hemodialysis is the most effective and rapid treatment for persistent, life-threatening hyperkalemia.
Hemodialysis may remove up to 25-50 mEq per hour.
K dialysate bath concentration: Avoid zero K bath, use 1 mEq/L concentrations with great caution and under continuous EKG monitoring.
. Table I Predialysis serum K Dialysate K Special considerations <4.0 4.0 4.0 to 4.5 3.5 4.6 to 5.5 3.0 2.0 if rapid interdialytic increase expected >5.5 but <8.0 2.0 Increase to 2.5 or 3 in patients at risk of arrhythmia or on digitalis
In patients with severe hyperkalemia greater than 8.0 mEq/L a dialyzate concentration of 1.0 can be used for a short period of time (i.e. 1 hour) to rapidly decrease K levels; switch to 2.0 K bath as soon as serum K levels reach 6-7 mEq/L.
Zero K bath is not recommended due to risk of severe arrhythmia.
Avoid excessively rapid correction of hyperkalemia to decrease risk of arrhythmia, keep patients under continuous EKG monitoring.
Potassium rebound: Immediate post-dialysis measurements of serum K are misleadingly low: if K rebounds, consider continuous renal replacement therapies; continuous renal replacement therapies slower for initial correction of hyperkalemia.
Management of hypomagnesemia
Severe symptomatic hypomagnesemia must be emergently treated to rise Mg above 1 mg/dl.
Total body Mg stores may not be reflected by serum Mg levels and may need prolonged treatment for complete replacement.
As serum Mg rises with treatment, significant ongoing renal loss may require additional treatment:
Serum Mg levels are the main regulator of renal Mg reabsorption in the loop of Henle: abrupt elevation in serum Mg will decrease Mg reabsorption and up to 50% of the infused dose may be lost in the urine.
Simultaneous K depletion must by replenished.
50 mEq intravenous magnesium slowly infused over 8-24 hours.
Magnesium sulphate 16-24 ml of 50% magnesium sulphate (64-96 mEq) in 500 ml 5% dextrose over 6-8 hours, may repeat every 12 hours.
In renal failure decrease dose to 1/2.
Mild to moderate:
Avoid factors inducing Mg loss.
Oral elemental Mg 10-20 mg/kg/dose up to 250-500 mg/dose given 3-4 times per day to avoid diarrhea.
Slow release preparations preferable: Slow Mag contains magnesium chloride and Mag-Tab SR contains magnesium lactate.
These preparations provide 5-7 mEq (2.5-3.5 mM or 60-84 mg) of elemental Mg per tablet.
Patients with thiazide- or loop diuretic-induced hypomagnesemia may benefit from a K-sparing diuretic such as amiloride.
Patients with chronic kidney disease:
Avoid Mg supplementation in patients with renal dysfunction unless magnesium-deplete (serum Mg<1 mg/dl).
Closely monitor Mg levels as Mg is repleted.
For patients with creatinine clearance 15-30 ml/min (CKD4) should receive 1/2 the usual dose of Mg.
Patients on chronic dialysis are rarely Mg depleted.
Management of hypermagnesemia
Magnesium overload should be avoided by limiting the intake of Mg-containing medications especially in patients with reduced kidney function.
Normal renal function:
Supportive treatment, hydration, loop diuretics.
Symptoms can be acutely reversed with intravenous Ca administration 100-200 mg IV infused over 5-10 minutes.
If levels are elevated in the face of renal dysfunction and hypermagnesemia is symptomatic, consider hemodialysis.
Special considerations for nursing and allied health professionals.
What's the evidence?
Mount, DB, Zandi-Nejad, K, Brenner, BM. "Disorders of potassium balance". Brenner and Rector's The Kidney. W.B. Saunders Co.. 2008. pp. 547.
Rose, BD, Post, TW, Rose, BD, Post, TW. "Hypokalemia". Ciinical physiology of acid base and electrolyte disorders. McGraw Hill. 2001. pp. 836.
Goilav, B, Trachtman, H, Feld, LG, Kaskel, FJ. "Disorders of potassium balance". Fluid and Electrolytes in Pediatrics. Humana Press, a part of Springer Science+Business Media. 2009. pp. 67.
Cerdá, J, Tolwani, A, Warnock, D. "Critical care nephrology: management of acid–base disorders with CRRT". Kidney Inl.. vol. 82. 1 July 2012. pp. 9-18.
Agus, ZS, Massry, SG, Narins, RG. "Hypomagnesemia and hypermagnesemia". Maxwell & Kleeman's Clinical Disorders of Fluid and Electrolyte Metabolism 5th Edition. McGraw-Hill. 1994. pp. 1099-119.
Reikes, S, Gonzalez, EA, Martin, KJ, DuBose, TD, Hamm, LL. "Abnormal calcium and magnesium metabolism". Acid Base and Electrolyte Disorders. Saunders. 2002. pp. 453-87.
Pollack, MR, Yu, ASL, Brenner, BM. "Clinical disturbances of calcium, magnesium and phosphate metabolism". Brenner and Rector's The Kidney. vol. 1. Saunders. 2004. pp. 535-71.
McKay, CP, Feld, LG, Kaskel, FJ. "Disorders of magnesium metabolism". Fluid and Electrolytes in Pediatrics. Humana Press, a part of Springer Science+Business Media. 2009. pp. 149.
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