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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2007  |  Volume : 18  |  Issue : 4  |  Page : 577-584
Hyperkalemia Revisited

Nephrology Department, King Fahad Specialist Hospital, Buraidah-Al Qassim, Saudi Arabia

Click here for correspondence address and email

Keywords: Electro-chemical gradients, Electrophysiology, Electrocardiography, Calcium exchange resins, Hyperkalemia, Calcium gluconate

How to cite this article:
Almukdad H. Hyperkalemia Revisited. Saudi J Kidney Dis Transpl 2007;18:577-84

How to cite this URL:
Almukdad H. Hyperkalemia Revisited. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2022 Aug 13];18:577-84. Available from: https://www.sjkdt.org/text.asp?2007/18/4/577/36515

   Introduction Top

Hyperakalemia is a common clinical and po­tentially life threatening metabolic problem that can induce deadly cardiac arrhythmias. It is caused by inability of the kidney to excrete potassium and/or impairment of the mecha­nisms that shift potassium from the circulation into the cells. Acute episodes of hyperkalemia are commonly triggered by the introduction of any medication that affects potassium homeo­stasis; an intercurrent illness or dehydration. In patients with diabetic kidney disease, hyper­kalemia may be caused by the hyporenine­mic hypoaldosteronism. The presence of typi­cal electrocardiographic changes or a rapid changes or a rapid rise in serum potassium le­vels usually indicates life threatening hyperka­lemia. Urine potassium, creatinine and osmo­larity should be obtained in order to determine the cause of hyperkalemia.

Intravenous calcium is effective in reversing the electrocardiographic changes and reducing the risk of arrhythmias but does not lower serum potassium. Serum potassium can be lowered acutely by using intravenous insulin and glucose and/or nebulized β2 agonist. So­dium polystyrene therapy, sometimes with intravenous furosemide and saline, can then be initiated to lower the total body potassium le­vels. The challenge in managing hyperkalemia stems from the fact that it can be difficult, if not impossible, to identify the condition solely on the basis of electrocardiographic informa­tion. This article reviews the electrophysiologic and electrocardiographic changes that occur as serum potassium levels increase, followed by discussion about the management of hyper­kalemia.

   Potassium Homeostasis Top

Extracellular potassium concentration is nor­mally maintained between 4.0 and 4.5 mmol/L by a complex interaction of potassium excre­tion and consumption. Ninety-five percent of total body potassium is intracellular, and only 2% is extracellular. A 70 kg man, for instance, has about 3920 mmols of potassium in the intracellular space. Considering the total daily intake of potassium from a normal diet is around 200 mmols, one can predict how pre­cisely and quickly the response of the body to any administered potassium load in order to prevent severe hyperkalemia.

Total body potassium levels are regulated mostly by the kidneys, with only 5% to 10% of ingested potassium excreted in the feces. [1] Renal excretion of potassium is determined by the rate of potassium filtration across the glo­merular basement membrane and by the rate of its secretion and resorption in the distal tubules of the nephron. Hyperkalemia may result when increased intake of potassium overwhelms the ability of the kidneys to excrete potassium, mainly when a decrease in renal function occurs.

Since there are often no specific clinical symptoms or signs to suggest hyperkalemia, clinicians must frequently rely on history of the case such as presence of renal failure or ingestion of medications known to cause hy­perkalemia, laboratory data and electrocardio­graphic changes to diagnose hyperkalemia.

   Effect of Hyperkalemia on Impulse Production and Propagation Top

Potassium and sodium concentrations in the intracellular and extracellular compart­ments play a vital role in the electrophysio­logic function of the myocardium. Concen­tration gradients are established across the myocyte membrane secondary to very high intracellular potassium concentrations and a relative paucity of potassium ions in the extra­cellular space. The opposite is true for sodium ions. These concentration gradients are main­tained by sodium-potassium adenosine tri­phosphatase (Na-K ATPase) pumps on the cellular walls, which actively pump sodium outward the myocyte and potassium inward. These concentration gradients establish an electrical potential across the cellular mem­brane that result in a resting membrane po­tential of -90 millivolts (mv). The potassium gradient across the cellular membrane is the most important factor in establishing this membrane potential; therefore, any changes in extracellular potassium concentration may have profound effects upon the myocyte electro­physiologic function. [2]

As potassium levels increase in extracel­lular space, the magnitude of the concentration gradient for potassium across the myocyte diminishes, thus decreasing the resting membrane potential (that is - 90 mv to -80 mv).

Phase O of the action potential occurs when voltage-gated sodium channels open and sodium enters the myocyte down its electro­chemical gradient [Figure - 1]. The rate of rise of phase O of the action potential (Vmax) is directly proportional to the value of the resting membrane potential at the onset of phase O.[3],[4] This is because the membrane potential at the onset of depolarization deter­mines the number of sodium channels that are activated during depolarization, which in turn determines the magnitude of the inward sodium current and the Vmax of the action potential. As illustrated in [Figure - 2], the per­centage of available sodium channels de­creases and the Vmax is greatest when the resting membrane potential at the onsent of the action potential is approximately -75 mV and it does not increase as the membrane potential becomes less negative (that is, -70 mV), as in the setting of hyperkalemia. This decrease results in a decrement in the inward sodium current and a concurrent decrease in the Vmax; therefore, as the resting membrane potential becomes less negative in hyper­kalemia, Vmax decreases. This decrease in Vmax causes slowing of impulse conduction through the myocardium and prolongation of membrane depolarization as a result, the QRS duration is prolonged.

As potassium levels increase further, the resting membrane potential continues to be less negative and thus progressively decreases Vmax. The decrease in Vmax, causes slowing of myocardial conduction, manifested by pro­gressive prolongation of the P waves, PR interval and QRS complex.

Hyperkalemia also has profound effects upon phase 2 and 3 of the action potential. After the rapid influx of sodium across the cell membrane in phase O, potassium ions leave the cell along its electrochemical gradient, which is reflected in phase 1 of the action po­tential. As the membrane potential attains -45 mV during phase O, calcium channels are stimulated, allowing calcium to enter the myocyte. The maximum conductance of these channels occurs approximately 50 m sec after the initiation of the phase O and is reflected in phase 2 of the action potential. During phase 2, potassium efflux and calcium influx offset one another so that the electrical change across the cell membrane remains the same and a plateau phase of the action potential is created [Figure - 1]. During phase 3, the calcium cha­nnels close, while the potassium channels con­tinue to efflux potassium out of the cell, Accordingly, the electronegative membrane potential is restored. [5]

The potassium currents (Ikr), located on the myocyte cell membrane, are mostly respon­sible for the potassium efflux seen during phase 2 and 3 of the cardiac action poten­tial. [6] For reasons that are not well unders­tood, these Ikr currents are sensitive to extra­cellular potassium levels and as the potassium levels increase in the extracellular space, potassium conductance through these currents is increased so that more potassium leaves the myocyte at any time. [6] This results in an in­crease in the slope of phases 2 and 3 of the action potential in patients with hyperkalemia and shortening of the repolarization. This is considered the mechanism responsible for some of the early electrocardiographic mani­festations of hyperkalemia, such as ST-T seg­ment depression, peaked T waves and Q-T interval shortening. [7],[8]

   Surface Electrocardiogram Manifestations of Hyperkalemia Top

In experimental models, there is a very orderly progression of electrocardiographic changes induced by hyperkalemia.[9],[10] The earliest electrocardiographic manifestation of hyperkalemia is the appearance of narrow­based, peaked T-waves. These T-waves are of relatively short duration, approximately 150 to 250 m sec, which helps distinguish them from the broad-based T waves typically seen in patients with myocardial infarction or intra­cerebral vascular accidents. [3] Peaked T waves are usually seen at potassium concentrations greater than 5.5 mmol/L and are best seen in leads II, III and V2 through V4, but are present in only 22% of patients with hyperkalemia. [7],[9],[10] Increased myocytes excita­bility, shortening of the myocyte action poten­tial and an increase in the slope of phase 2 and 3 of the action potential may account for the T wave peaking observed in mild hyperkalemia. [7]

Once serum potassium levels increase to greater than 6.5 mmol/L, the rate of phase O of the action potential decreases, which results in longer action potential, widened QRS com­plex and prolonged PR interval. Electro­physiologically, this appears as delayed intra­venticular conduction. As the intraventricular conduction delay worsens, the QRS complex may mimic that of left or right bundle branch block configuration. A clue that these electro­cardiographic changes are due to hyper­kalemia and not to bundle branch disease, is that in hyperkalemia the conduction delay persists throughout the QRS complex and not just in the initial or terminal portions as seen in left and right bundle branch block, respect­ively. [7],[11]

When potassium level reaches 8-9 mmol/L, the sinoatrial (SA) node activity may stimu­late the ventricles without evidence of atrial activity, producing a sinoventricular rhythm. This occurs because the SA node is less sus­ceptible to the effect of hyperkalemia and can continue to stimulate the ventricles without evidence of atrial electrical activity.[7],[12] The electrocardiographic manifestations of conti­nued SA node function in the absence of atrial activity may be very similar to those of ven­tricular tachycardia, given the absence of P waves and a widened QRS complex.

As the hyperkalemia worsens and potassium levels attain 10 mmol/L, the SA conduction no longer exists and passive junctional pacemaker supervene the electrical stimulation of the myo­cardium (accelerated junctional rhythm).[7],[8],[13] If hyperkalemia continue unabated, the QRS complex will continue to widen and even­tually blends with the T waves producing the classic sine-wave. Once this occurs, ventri­cular fibrillation and asystole are imminent.

Many other electrocardiographic abnorma­lities have been associated with hyperka­lemia. In patients with acutely elevated serum potassium levels, a pseudomyocardial infarct­tion pattern has been reported to appear as massive ST-T segment elevation that develops secondary to derangement in myocyte repo­larization. [14],[15] early stages of hyperkalemia may manifest with only shortening of the PR and QT interval.[16] Furthermore, sinus tachy­cardia, bradycardia, idioventricular rhythm and 1st -, 2nd - and 3rd degree heart block have all been described.

Due to the vast array of electrocardiographic manifestations of hyperkalemia, the difficulty in consistently identifying hyperkalemia on the basis of electrocardiographic abnormalities and the progression of the electrocardiogram during hyperkalemia from normal to that of ventricular tachycardia and asystole precipi­tously, physicians need to consider this diag­nosis in patients at risk. [16]

   Causes of Hyperkalemia Top

In many patients, the cause of hyperkalemia is multifactorial and never clearly defined. The most common causes of hyperkalemia are renal diseases and ingestion of medications that predispose patients to hyperkalemia. [17] Medications known to cause hyperkalemia include angiotensin-converting enzyme inhi­bitors, angiotensin-receptor blockers, penicillin G, trimethoprim, spironolactone, succinyl­choline, alternative medicines and Heparin, to name just a few.[18],[19]

Acker et al,[17] reported that 75% of patients with severe hyperkalemia had renal failure and 67% were on a predisposing drug. Other less commonly reported causes of hyperkalemia include massive crushing injury with resultant muscle damage, large burns, high-volume blood transfusions, human immunodeficiency virus infection and tumorlysis syndrome.[16],[20],[21]

   Treatment of Hyperkalemia Top

Sometimes, physicians initiate treatment for hyperkalemia on the basis of a patient's clini­cal scenario such as a cardiac arrest that occurs in a chronic dialysis patient. However, more commonly the patient is treated when labo­ratory data become available. Most authorities recommend treatment for hyperkalemia when electrocardiographic changes are present or when serum potassium levels are greater than 6.5 mmol/L, regardless of the electrocardio­gram.[22],[23]

Treatment for hyperkalemia can be catego­rized into three distinct steps. First, antago­nization of the effects of hyperkalemia at the cellular level (membrane stabilization), second; decrease of serum potassium levels by pro­motion of influx of potassium into cells throughout the body and third; remove pota­ssium from the body.

a) Membrane stabilization : The initial treat­ment of hyperkalemia should be the infusion of calcium. Calcium antagonizes the effects of hyperkalemia at the cellular level through three major mechanisms that include resetting the resting membrane potential to a less nega­tive value, closer to the normal threshold po­tential of -75 mV, so the difference between the resting and threshold potentials of 15 mv can be restored.[24] Second, it has been de­monstrated in animal studies that increasing level of calcium shifts the curve relating Vmax to the resting membrane potential at the onset of action potential upward and to the right [Figure - 3]. [4] Therefore, at any given level of resting membrane potential, up to approxi­mately -75 mV, the Vmax is increased when high calcium concentrations are present. [25] This serves to return myocyte excitability back to normal in the setting of hyperkalemia. Finally, in cells with calcium-dependent action poten­tials, such as SA and atrioventricular nodal cells and in cells in which the sodium current is depressed, an increase in extracellular calcium concentration increases the magnitude of the calcium inward current and the Vmax by increasing the electrochemical gradient across the myocyte. This speeds the impulse propagation in such tissues, reversing the myocyte depression observed with hyper­kalemia. [26]

The effect of intravenous calcium occurs within 1 to 3 minutes but lasts for only 30 to 60 minutes, so further, more definitive treat­ment is required to lower serum potassium le­vels. Calcium gluconate is the preferred preparation of intravenous calcium. The dose should be 10 ml of a 10% calcium gluconate solution infused over 2 to 3 minutes. Calcium chloride may also be used but provides about three times the amount of calcium per 10 ml dose, so the dose needs to be attenuated accordingly to avoid potential calcium toxicity. [22]

Since hyperkalemia can potentiate digitalis toxicity, calcium should be used in patients on this drug only if there is loss of P waves or a widened QRS complexes.[6] In this situation, calcium gluconate should be diluted in 100 ml of D5W and infused over 30 minutes.

b) Potassium Influx into Cells : This is most frequently done by administration of insulin, which stimulates the Na-K ATPase pump, that in turn moves potassium intracellularly in ex­change for sodium in a 2:3 ratio; this effect is independent of insulin's effect on glucose.[27] Ten units of intravenous Insulin is typically infused, followed by close monitoring of serum blood glucose. Fifty mL of 50% dextrose is frequently co-administered with insulin in nor­moglycemic patients to prevent hypoglycemia. If a patient is already hyperglycemic, supple­mental glucose is not needed. The effect of insulin is observed within 10 to 20 minutes of administration and can be expected to decrease potassium levels by 0.6 to 1.0 mmol/L.[22],[28],[29],[30]

Increasing evidence suggests that there may be a role for albuterol in the treatment of patients with severe hyperkalemia, since cate­cholamines activate Na-K ATPase pumps through β2 receptor stimulation in a manner that is additive to the effect of insulin.[22],[20] In a study by Montolin and Coworkers,[27] 0.5 mg of intravenous albuterol was infused in patients with hyperkalemia that resulted in a 1-mmol/L decrease in serum potassium levels with minimal adverse effects.[27] Because there are no approved intravenous form of β2 ago­nists available in the United States, studies have been performed to deter-mine whether nebulized β2 -agonist would have a similar effect on serum potassium levels. One such study found that albuterol, when administered in very high doses (10-20 mg), decreased potassium levels by 0.62 to 0.98 mmol/L.[31] The onset of action for inhaled albuterol was immediate and lasted for 1 to 2 hours. There­fore, β2 agonist therapy should be considered as an adjunctive treatment for patients with severe hyperkalemia.

Sodium bicarbonate infusion can shift po­tassium from the extracellular to intracellular space by increasing blood PH. However, rou­tine bicarbonate therapy for the treatment of hyperkalemia is controversial.[22],[32],[33]

In a study by Blumberg and associates,[34] 12 dialysis patients with potassium levels of 5.25 to 8.15 mmol/L, received 390 mmol of intra­venous sodium bicarbonate over a six-hour period. No change in potassium levels was observed until four hours after drug adminis­tration, with a decrease of 0.7 mmol/L.[34] Due to the lack of a quick or sustained decrement in potassium levels, physicians should reserve the use of intravenous sodium bicarbonate for situations wherein severe acidemia or pheno­barbital and tricyclic anti-depressant overdose is present

c) Potassium Removal from the Body : hemodialysis is the quickest and most effi­cient remove potassium.[28] In 1970, Morgan et al,[35] reported the removal of 48 mmol of potassium using a KiiL dialyzer over a 10­hour period; others confirmed these findings. [35],[36],[37] However, because of the time, expense and invasive nature of hemodialysis therapy, it is rarely used as a first line treatment for hyperkalemia unless a patient is already on dialysis and has life threatening hyper­kalemia.

Ion exchange resins can be administered orally or rectally and function by exchanging gut cations, most importantly potassium, for sodium ions that are released from the resin. Most studies have found exchange resins to decrease serum potassium level by about 1 mmol/L over a 24-hour period.[38] It should be emphasized that the extended time required for exchange resins to exert effect excludes their use in the emergent treatment of hyper­kalemia. Exchange resins can cause significant constipation and are typically administered in combination with a laxative such as sorbitol, which prevents constipation and promotes the elimination of potassium from the gut once it binds to the resin.

Although generally safe, the combination of a resin and sorbitol has been reported to cause intestinal necrosis and accordingly should be used cautiously and only when necessary.[39],[40]

   References Top

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2.Dananberg J. Electrolyte abnormalities affecting the heart. In: Schwartz GR, ed. Principles and practice of emergency medicine. 4th ed. Baltimore: Williams and Wilkins; 1999; p. 425-7.  Back to cited text no. 2    
3.Szerlip HM, Weiss J,Singer I. Profound hyperkalemia without electrocardiographic manifestations. Am J Kidney Dis 1986;7: 461-5.  Back to cited text no. 3  [PUBMED]  
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28.Blumberg A, Weidmann P, Shaw S, Gnadinger M. Effect of various thera-peutic approaches on plasma potassium and major regulating factors in terminal renal failure. Am J Med 1988;85:507-12.  Back to cited text no. 28    
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32.Kamel KS, Halperin ML, Faber MD, Steigerwalt SP, Heilig CW, Narins RG. Disorders of potassium balance. In: Brenner BM, Rector FC, eds. Brenner and Rector's the kidney. 5th ed. Philadelphia: WB Saunders; 1996. p. 999-1037.  Back to cited text no. 32    
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37.Sherman RA, Hwang ER, Bernhole AS, Eisinger RP. Variability in potassium removal by haemodialysis. Am J Nephrol 1986;6: 284-8.  Back to cited text no. 37    
38.Scherr L, Ogden DA, Mead AW, Spritz N, Rubin AL. Management of hyper-kalemia with a cation-exchange resin. N Engl J Med 1961;264:115-9.  Back to cited text no. 38  [PUBMED]  
39.Gerstman BB, Kirkman R, Platt R. Intestinal necrosis associated with post­operative orally administered sodium poly­styrene sulfonate in sorbitol. Am J Kidney Dis 1992;20:159-61.  Back to cited text no. 39  [PUBMED]  
40.Dardik A, Moesinger RC, Efron G, Barbul A, Harrison MG. Acute abdomen with colonic necrosis induced by Kayexalate­sorbitol. South Med J 2000;93:511-3.  Back to cited text no. 40  [PUBMED]  

Correspondence Address:
Hashem Almukdad
Consultant Nephrologist, King Fahad Specialist Hospital, P.O. Box 2290, Buraidah-Al Qassim
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 17951946

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