5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

Official reprint from UpToDate®

www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Clinical manifestations of hyperkalemia in adults

AUTHOR: David B Mount, MD
SECTION EDITOR: Richard H Sterns, MD
DEPUTY EDITOR: John P Forman, MD, MSc

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2024.

This topic last updated: Dec 07, 2022.

INTRODUCTION

Hyperkalemia is a common clinical problem that is most often due to impaired urinary
potassium excretion due to acute or chronic kidney disease and/or disorders or drugs that
inhibit the renin-angiotensin-aldosterone axis. Therapy for hyperkalemia due to potassium
retention is ultimately aimed at inducing potassium loss [1-3]. In some cases, the primary
problem is movement of potassium out of the cells, even though the total body potassium
may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled
hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). (See
"Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section
on 'Potassium replacement'.)

The clinical manifestations of hyperkalemia will be reviewed here. The causes, diagnosis,
treatment, and prevention of hyperkalemia are discussed separately. (See "Causes and
evaluation of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in
adults".)

CLINICAL MANIFESTATIONS

The most serious manifestations of hyperkalemia are muscle weakness or paralysis, cardiac
conduction abnormalities, and cardiac arrhythmias [4]. These manifestations usually occur
when the serum potassium concentration is ≥7.0 mEq/L with chronic hyperkalemia or
possibly at lower levels with an acute rise in serum potassium. Patients with skeletal muscle
or cardiac manifestations typically have one or more of the characteristic ECG abnormalities
associated with hyperkalemia.

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 1/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

Other manifestations in hyperkalemic patients may be related to the cause of the

hyperkalemia, such as polyuria and polydipsia with uncontrolled diabetes.

Severe muscle weakness or paralysis — Hyperkalemia can cause ascending muscle

weakness that begins with the legs and progresses to the trunk and arms [5-7]. This can
progress to flaccid paralysis, mimicking Guillain-Barré syndrome [6,7]. Sphincter tone and
cranial nerve function are typically intact, and respiratory muscle weakness is rare [8]. These
manifestations resolve with correction of the hyperkalemia.

In addition to acquired hyperkalemia, there is a genetic disorder hyperkalemic periodic

paralysis that is caused by autosomal dominant mutations in the skeletal muscle cell sodium
channel. Patients with this disorder develop myopathic weakness during hyperkalemia
induced by increased potassium intake or rest after heavy exercise. (See "Hyperkalemic
periodic paralysis".)

Cardiac manifestations — Hyperkalemia may be associated with electrocardiographic

changes that, if present, may suggest the diagnosis before blood test results. Other
manifestations include conduction abnormalities and cardiac arrhythmias.

ECG changes — Hyperkalemia may be associated with a variety of changes on the

electrocardiogram (ECG). Tall peaked T waves with a shortened QT interval are usually the
first findings ( waveform 1). As the hyperkalemia becomes more severe, there is
progressive lengthening of the PR interval and QRS duration, the P wave may disappear, and
ultimately the QRS widens further to a sine wave pattern. Ventricular standstill with a flat line
on the ECG ensues with complete absence of electrical activity. ECG manifestations can
evolve rapidly and unpredictably [9].

The presence of ECG changes in patients with hyperkalemia indicates an increased risk of
adverse events. For example, in one study of 188 patients with serum potassium >6.5 mEq/L,
all patients who had an acute adverse cardiac event (ie, symptomatic bradycardia, ventricular
tachycardia, ventricular fibrillation, cardiopulmonary resuscitation, and/or death) had a
preceding ECG that demonstrated at least one hyperkalemic abnormality [10].

The progression and severity of ECG changes do not correlate well with the serum potassium
concentration as illustrated by the following observations:

● In a review of 90 patients with hyperkalemia (80 percent with a serum potassium below
7.2 mEq/L), the probability of ECG abnormalities increased with increasing serum
potassium, but the ECG was insensitive for the diagnosis of hyperkalemia [11].

● In another report, the prevalence of ECG changes suggestive of hyperkalemia was

independent of severity (43 and 55 percent in patients with a serum potassium less
than 6.8 mEq/L and those with higher values, respectively) [12].

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 2/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

● Rare patients have a normal ECG despite a serum potassium above 9.0 mEq/L [13].

● ECG manifestations are more likely with rapid onset hyperkalemia [14] and the
presence of concomitant hypocalcemia, acidemia, and/or hyponatremia [11,15].

Given the unreliable sensitivity, serial measurements of the serum potassium concentration
should guide therapy in stable patients with hyperkalemia. The ECG cannot be reliably used
to monitor the efficacy of hyperkalemia therapy [13]. In addition, peaked T waves alone are
not specific for hyperkalemia, being seen in the early phase of acute myocardial infarction
and with early repolarization, and some patients with left ventricular hypertrophy ( table 1)
[16,17].

Hyperkalemia can also cause a type I Brugada pattern in the ECG, with a pseudo-right
bundle branch block and persistent "coved" ST segment elevation in at least two precordial
leads. This "hyperkalemic Brugada sign" occurs in critically ill patients with significant
hyperkalemia (serum potassium concentration >7.0 mEq/L), and can be differentiated from
genetic Brugada syndrome by an absence of P waves, marked QRS widening, and/or an
abnormal QRS axis [18]. (See "Brugada syndrome: Clinical presentation, diagnosis, and
evaluation".)

Conduction abnormalities and arrhythmias — Hyperkalemia can lead to a variety of

conduction abnormalities and arrhythmias:

● Conduction abnormalities that may be seen include right bundle branch block, left
bundle branch block, bifascicular block, and advanced atrioventricular block [19].

● Cardiac arrhythmias associated with hyperkalemia include sinus bradycardia, sinus

arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and
asystole [20-22].

Cardiac death — Hyperkalemia increases the risk of mortality in multiple patient

populations, including patients with and without preexisting cardiovascular disease [23,24],
patients with various severities of chronic kidney disease [25-30], and critically ill hospitalized
patients [31,32]. Rapid-onset hyperkalemia may be more lethal than hyperkalemia that
develops more slowly [4,14,33]. [26-32] The cause of excess mortality in hyperkalemia is likely
multifactorial, but clearly arrhythmia plays an important role [4,34].

In patients who present to the emergency department with hyperkalemia and in those who
develop hyperkalemia in the intensive care unit, early correction of the serum potassium is
associated with reduced mortality [4,31,32,34-36].

Reduced urinary acid excretion — Hyperkalemia interferes with renal ammonium (NH4+)
excretion, thereby limiting acid excretion and possibly leading to the development of

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 3/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

metabolic acidosis [37-41]. This association has been well described in humans as illustrated
by the following observations; similar findings have been described in animal models [41]:

● Two case reports described patients with isolated hyporeninemic hypoaldosteronism

and mild to moderate chronic kidney disease who had hyperkalemia, metabolic
acidosis, and reduced urinary NH4+ excretion [38]. Correction of the hyperkalemia with
a potassium-sodium exchange resin led to resolution of the acidemia and normalization
of urinary NH4+ excretion.

● In a study in normal men, ingesting a high potassium diet for five days was associated
with a significant reduction in both ammonium and net acid excretion [40].

● Correction of hyperkalemia with the potassium binder ZS-9 is associated with an

increase in the serum bicarbonate concentration [42,43]. However, in addition to
potential indirect effects on renal ammonium excretion, ZS-9 binds intestinal
ammonium [44].

At least three mechanisms are thought to contribute to the hyperkalemia-induced

diminution in ammonium secretion:

● An intracellular alkalosis as entry of some of the excess potassium into the cells is
associated with hydrogen ion movement out the cells to maintain electroneutrality. The
intracellular alkalosis will reduce both ammonium excretion and bicarbonate
reabsorption [38,40,41,45,46].

● Reduced NH4+ reabsorption in the thick ascending limb of the loop of Henle [41,47]. In
normal subjects, NH4+ can substitute for potassium on the Na-K-2Cl cotransporter in
the luminal membrane, a process that is essential for medullary recycling of NH4+,
which is subsequently secreted into the medullary collecting duct [48]. With
hyperkalemia, potassium competes with NH4+ for transport by the Na-K-2Cl
cotransporter, resulting in reductions in medullary recycling and NH4+ secretion and
the development of metabolic acidosis. Hyperkalemia also reduces expression of the
ammonia transporter Rhcg in the inner stripe of the outer medulla of hyperkalemic
animals, thereby reducing ammonia transport across the collecting duct [49].

● Diminished proximal tubular ammoniagenesis, mediated in part by reduced glutamine

deamination [50]. Hyperkalemia reduces expression of the ammonia-generating
enzymes phosphate-dependent glutaminase and phosphoenolpyruvate carboxykinase,
along with overexpression of the ammonia-recycling enzyme glutamine synthetase
[49]; these changes are reversed by normokalemia.

PATHOGENESIS
https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 4/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

The muscle weakness and cardiac manifestations induced by hyperkalemia are related to
impaired neuromuscular transmission [2,51]. The generation of an action potential (called
membrane excitability) is related both to the magnitude of the resting membrane potential
and to the activation state of membrane sodium channels. Opening of these sodium
channels, leading to the passive diffusion of extracellular sodium into the cells, is the primary
step in this process.

According to the Nernst equation, the resting electrical potential across the cell membrane is
related to the ratio of the extracellular to intracellular potassium concentration. An elevation
in the extracellular (plasma) potassium concentration decreases this ratio; makes the resting
potential less electronegative and partially depolarizing the cell membrane.

The less negative resting potential will initially increase membrane excitability since a lesser
depolarizing stimulus is required to generate an action potential. However, the later effect is
different. Persistent depolarization inactivates sodium channels in the cell membrane,
thereby producing a net decrease in membrane excitability that may be manifested clinically
by impaired cardiac conduction and/or neuromuscular weakness or paralysis [51].

Increases in extracellular potassium also affect the repolarization phase of the cardiac action
potential via activation of the rapidly activating delayed rectifier potassium channel (IKr). The
HERG (human ether-a-go-go-related) gene encodes the pore-forming subunits of IKr, which is
largely responsible for potassium efflux during phases 2 and 3 of the cardiac action potential
[34]. HERG channels are highly sensitive to changes in extracellular potassium, with
inhibition in hypokalemia and activation during hyperkalemia [52,53]. This effect of
hyperkalemia on repolarization is thought to underlie the "early" signs of hyperkalemia [21],
including ST-T segment depression, peaked T waves, and QT interval shortening [34].

PATIENT ASSESSMENT

Careful monitoring of the ECG and muscle strength are indicated to assess the functional
consequences of hyperkalemia. Severe muscle weakness and/or marked
electrocardiographic changes, including conduction abnormalities and arrhythmias, are
potentially life-threatening and require immediate treatment. These manifestations usually
occur when the serum potassium concentration is ≥7.0 mEq/L with chronic hyperkalemia or
possibly at lower levels with an acute rise in serum potassium. (See "ECG tutorial:
Miscellaneous diagnoses", section on 'Hyperkalemia'.)

Rapid increases in serum potassium cause more pronounced cardiac toxicity [33], with
greater apparent effects on mortality [4]. A careful history should assess the probable cause
of the hyperkalemia (eg, tissue breakdown) and the expected rate of change in serum

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 5/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

potassium; treatment should be adjusted accordingly [54]. (See "Treatment and prevention
of hyperkalemia in adults".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Fluid and electrolyte
disorders in adults".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Hyperkalemia (The Basics)")

SUMMARY

● The most serious manifestations of hyperkalemia are ascending muscle weakness or

paralysis, cardiac conduction abnormalities, and cardiac arrhythmias. These usually
occur when the serum potassium concentration is ≥7.0 mEq/L if hyperkalemia is chronic
or lower if hyperkalemia is acute. (See 'Clinical manifestations' above.)

● Electrocardiogram (ECG) changes associated with hyperkalemia include tall peaked T

waves with a shortened QT interval; progressive lengthening of the PR interval and QRS
duration; disappearance of the P wave; and widening of the QRS complex to a sine
wave pattern. The progression and severity of ECG changes do not correlate well with
the serum potassium concentration. (See 'ECG changes' above.)

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 6/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

● Conduction abnormalities associated with hyperkalemia include right bundle branch

block, left bundle branch block, bifascicular block, and advanced atrioventricular block.
Cardiac arrhythmias associated with hyperkalemia include sinus bradycardia, sinus
arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and
asystole. (See 'Conduction abnormalities and arrhythmias' above.)

● Hyperkalemia may cause metabolic acidosis by interfering with renal ammonium

(NH4+) excretion. (See 'Reduced urinary acid excretion' above.)

● The functional consequences of hyperkalemia are assessed by careful monitoring of the

ECG and muscle strength. Severe muscle weakness and/or marked electrocardiographic
changes may require immediate treatment. Rapid increases in serum potassium cause
more pronounced cardiac toxicity. (See 'Patient assessment' above.)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

1. Mount DB, Zandi-Nejad K. Disorders of potassium balance. In: Brenner and Rector's The
Kidney, 11th ed, Brenner BM (Ed), WB Saunders Co, Philadelphia 2020. p.537.
2. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, Mc-
Graw Hill, New York 2001. p.913.
3. Kamel KS, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol Dial
Transplant 2003; 18:2215.
4. Montford JR, Linas S. How Dangerous Is Hyperkalemia? J Am Soc Nephrol 2017; 28:3155.

5. FINCH CA, SAWYER CG, FLYNN JM. Clinical syndrome of potassium intoxication. Am J Med
1946; 1:337.
6. Evers S, Engelien A, Karsch V, Hund M. Secondary hyperkalaemic paralysis. J Neurol
Neurosurg Psychiatry 1998; 64:249.
7. BELL H, HAYES WL, VOSBURGH J. HYPERKALEMIC PARALYSIS DUE TO ADRENAL
INSUFFICIENCY. Arch Intern Med 1965; 115:418.

8. Freeman SJ, Fale AD. Muscular paralysis and ventilatory failure caused by hyperkalaemia.
Br J Anaesth 1993; 70:226.

9. Glober N, Burns BD, Tainter CR. Rapid Electrocardiogram Evolution in a Dialysis Patient. J
Emerg Med 2016; 50:497.
10. Durfey N, Lehnhof B, Bergeson A, et al. Severe Hyperkalemia: Can the Electrocardiogram
Risk Stratify for Short-term Adverse Events? West J Emerg Med 2017; 18:963.

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 7/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

11. Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG
changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324.

12. Acker CG, Johnson JP, Palevsky PM, Greenberg A. Hyperkalemia in hospitalized patients:
causes, adequacy of treatment, and results of an attempt to improve physician
compliance with published therapy guidelines. Arch Intern Med 1998; 158:917.

13. Szerlip HM, Weiss J, Singer I. Profound hyperkalemia without electrocardiographic

manifestations. Am J Kidney Dis 1986; 7:461.

14. Surawicz B, Chlebus H, Mazzoleni A. Hemodynamic and electrocardiographic effects of

hyperpotassemia. Differences in response to slow and rapid increases in concentration
of plasma K. Am Heart J 1967; 73:647.
15. Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially
lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant 2002; 17:1639.
16. Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave: electrocardiographic
differential diagnosis. Am J Emerg Med 2002; 20:243.

17. Arnsdorf MF. Electrocardiogram in Hyperkalemia: electrocardiographic pattern of

anteroseptal myocardial infarction mimicked by hyperkalemia-induced disturbance of
impulse conduction. Arch Intern Med 1976; 136:1161.

18. Littmann L, Monroe MH, Taylor L 3rd, Brearley WD Jr. The hyperkalemic Brugada sign. J
Electrocardiol 2007; 40:53.

19. Bashour T, Hsu I, Gorfinkel HJ, et al. Atrioventricular and intraventricular conduction in
hyperkalemia. Am J Cardiol 1975; 35:199.
20. Greenberg A. Hyperkalemia: treatment options. Semin Nephrol 1998; 18:46.

21. Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia.

Am J Emerg Med 2000; 18:721.

22. Drumheller BC, Tuffy E, Gibney F, et al. Severe bradycardia from severe hyperkalemia:
Patient characteristics, outcomes and factors associated with hemodynamic support.
Am J Emerg Med 2022; 55:117.

23. Grodzinsky A, Goyal A, Gosch K, et al. Prevalence and Prognosis of Hyperkalemia in

Patients with Acute Myocardial Infarction. Am J Med 2016; 129:858.
24. Horne L, Ashfaq A, MacLachlan S, et al. Epidemiology and health outcomes associated
with hyperkalemia in a primary care setting in England. BMC Nephrol 2019; 20:85.
25. Collins AJ, Pitt B, Reaven N, et al. Association of Serum Potassium with All-Cause
Mortality in Patients with and without Heart Failure, Chronic Kidney Disease, and/or
Diabetes. Am J Nephrol 2017; 46:213.
26. Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, et al. Impact of admission
serum potassium on mortality in patients with chronic kidney disease and

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 8/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

cardiovascular disease. QJM 2017; 110:713.

27. Gorriz JL, D'Marco L, Pastor-González A, et al. Long-term mortality and trajectory of
potassium measurements following an episode of acute severe hyperkalaemia. Nephrol
Dial Transplant 2022; 37:522.

28. Kovesdy CP, Matsushita K, Sang Y, et al. Serum potassium and adverse outcomes across
the range of kidney function: a CKD Prognosis Consortium meta-analysis. Eur Heart J
2018; 39:1535.

29. Brunelli SM, Du Mond C, Oestreicher N, et al. Serum Potassium and Short-term Clinical
Outcomes Among Hemodialysis Patients: Impact of the Long Interdialytic Interval. Am J
Kidney Dis 2017; 70:21.

30. Kovesdy CP, Regidor DL, Mehrotra R, et al. Serum and dialysate potassium
concentrations and survival in hemodialysis patients. Clin J Am Soc Nephrol 2007; 2:999.
31. McMahon GM, Mendu ML, Gibbons FK, Christopher KB. Association between
hyperkalemia at critical care initiation and mortality. Intensive Care Med 2012; 38:1834.
32. Bouadma L, Mankikian S, Darmon M, et al. Influence of dyskalemia at admission and
early dyskalemia correction on survival and cardiac events of critically ill patients. Crit
Care 2019; 23:415.
33. Paice B, Gray JM, McBride D, et al. Hyperkalaemia in patients in hospital. Br Med J (Clin
Res Ed) 1983; 286:1189.
34. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart
Inst J 2006; 33:40.

35. Singer AJ, Thode HC Jr, Peacock WF. Rapid correction of hyperkalemia is associated with
reduced mortality in ED patients. Am J Emerg Med 2020; 38:2361.
36. An JN, Lee JP, Jeon HJ, et al. Severe hyperkalemia requiring hospitalization: predictors of
mortality. Crit Care 2012; 16:R225.
37. Karet FE. Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol 2009;
20:251.
38. Szylman P, Better OS, Chaimowitz C, Rosler A. Role of hyperkalemia in the metabolic
acidosis of isolated hypoaldosteronism. N Engl J Med 1976; 294:361.

39. Matsuda O, Nonoguchi H, Tomita K, et al. Primary role of hyperkalemia in the acidosis of
hyporeninemic hypoaldosteronism. Nephron 1988; 49:203.

40. Tannen RL, Wedell E, Moore R. Renal adaptation to a high potassium intake. The role of
hydrogen ion. J Clin Invest 1973; 52:2089.
41. DuBose TD Jr, Good DW. Effects of chronic hyperkalemia on renal production and
proximal tubule transport of ammonium in rats. Am J Physiol 1991; 260:F680.

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&selecte… 9/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

42. de Francisco A, Rasmussen H, Lavin P, et al. Normalization of serum bicarbonate with

sodium zirconium cyclosilicate (ZS-9) in the Phase 3 randomized, double-blind, placebo-
controlled HARMONIZE study. Nephrol Dial Transplant 2015; 30:iii6.
43. Ash SR, Singh B, Lavin PT, et al. A phase 2 study on the treatment of hyperkalemia in
patients with chronic kidney disease suggests that the selective potassium trap, ZS-9, is
safe and efficient. Kidney Int 2015; 88:404.
44. Stavros F, Yang A, Leon A, et al. Characterization of structure and function of ZS-9, a K+
selective ion trap. PLoS One 2014; 9:e114686.
45. FULLER GR, MACLEOD MB, PITTS RF. Influence of administration of potassium salts on
the renal tubular reabsorption of bicarbonate. Am J Physiol 1955; 182:111.
46. Jaeger P, Karlmark B, Giebisch G. Ammonium transport in rat cortical tubule: relationship
to potassium metabolism. Am J Physiol 1983; 245:F593.
47. DuBose TD Jr, Good DW. Chronic hyperkalemia impairs ammonium transport and
accumulation in the inner medulla of the rat. J Clin Invest 1992; 90:1443.
48. Good DW. Ammonium transport by the thick ascending limb of Henle's loop. Annu Rev
Physiol 1994; 56:623.

49. Harris AN, Grimm PR, Lee HW, et al. Mechanism of Hyperkalemia-Induced Metabolic
Acidosis. J Am Soc Nephrol 2018; 29:1411.

50. Sleeper RS, Belanger P, Lemieux G, Preuss HG. Effects of in vitro potassium on
ammoniagenesis in rat and canine kidney tissue. Kidney Int 1982; 21:345.

51. Berne RM, Levy MN. Cardiovascular Physiology, 4th ed, Mosby, St. Louis 1981.

52. Guo J, Massaeli H, Xu J, et al. Extracellular K+ concentration controls cell surface density
of IKr in rabbit hearts and of the HERG channel in human cell lines. J Clin Invest 2009;
119:2745.

53. Sanguinetti MC, Jiang C, Curran ME, Keating MT. A mechanistic link between an inherited
and an acquired cardiac arrhythmia: HERG encodes the IKr potassium channel. Cell
1995; 81:299.

54. Charytan D, Goldfarb DS. Indications for hospitalization of patients with hyperkalemia.
Arch Intern Med 2000; 160:1605.
Topic 2342 Version 22.0

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&select… 10/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

GRAPHICS

Peaked T waves as first sign of hyperkalemia on electrocardiogram

A tall peaked and symmetrical T wave is the first change seen on the electrocardiogram in a patient
with hyperkalemia.

Graphic 80441 Version 7.0

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&select… 11/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

Causes of tall (peaked) T waves on ECG

Ischemic causes

Hyperacute phase of myocardial infarction

Acute transient transmural ischemia (Prinzmetal's angina)

Chronic (evolving) phase of myocardial infarction (tall positive T waves reciprocal to primary deep T
wave inversions)

Nonischemic causes

Normal variants ("early repolarization" patterns)

Hyperkalemia

Acute hemopericardium

Cerebrovascular hemorrhage (more commonly T wave inversions)

Left ventricular hypertrophy

Right precordial leads, usually in conjunction with left precordial ST depressions and T wave
inversions

Left precordial leads, particularly in association with "diastolic" volume overload conditions

Left bundle branch block (right precordial leads)

Acute pericarditis (occasionally)

ECG: electrocardiogram.

Graphic 73040 Version 3.0

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&select… 12/13
5/30/24, 11:32 PM Clinical manifestations of hyperkalemia in adults - UpToDate

Contributor Disclosures
David B Mount, MD Consultant/Advisory Boards: Amgen [Gout therapeutics, vasculitis therapeutics];
Horizon Therapeutics [Gout therapeutics]. All of the relevant financial relationships listed have been
mitigated. Richard H Sterns, MD No relevant financial relationship(s) with ineligible companies to
disclose. John P Forman, MD, MSc No relevant financial relationship(s) with ineligible companies to
disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

https://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults/print?search=hyperkalemia&source=search_result&select… 13/13