Potassium
Hyperkalemia
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Hyperkalemia
, Hyperkalemia Related EKG Changes
See Also
Hyperkalemia Causes
Hyperkalemia Management
Pathophysiology
See
Potassium Homeostasis
Images
Epidemiology
Prevalence
Gene
ral population: 3.3%
Emergency Department: 3.6%
Chronic Kidney Disease
: 18%
Inpatient: 6.9 to 12.3%
Brookes (2021) Intern Med J 51(11): 1906-18 [PubMed]
Kovesdy (2018) Eur Heart J 39(17): 1535-42 [PubMed]
Singer (2017) Clin Exp Emerg Med 4(2): 73-9 [PubMed]
Causes
See
Hyperkalemia Causes
Findings
Signs and Symptoms
Symptoms occur when
Serum Potassium
> 6.0 to 6.5 meq/L
Neurologic Changes
Weakness
Paresthesia
s
Areflexia
Ascending paralysis
Respiratory Failure
Cardiovascular Changes
Bradycardia
to
Asystole
or
Ventricular Fibrillation
AV prolonged transmission to complete
Heart Block
Labs
Chemistry Panel
Serum Potassium
Serum
Electrolyte
s including serum bicarbonate
Renal Function
tests (BUN,
Creatinine
)
Spot urine for
Urine Potassium
,
Urine Sodium
and
Urine Creatinine
Fractional Excretion of Potassium
Transtubular Potassium Gradient
Urine Sodium
<25 mEq/L suggests decreased distal renal flow
See
Hyperkalemia Causes
Other labs to consider (see evaluation below)
Serum
Aldosterone
Serum renin
Diagnostics
Electrocardiogram
Gene
ral
EKG changes occur when
Serum Potassium
>6.0 meq/L
EKG may however be normal despite significant Hyperkalemia
When significant EKG changes are present, pursue aggressive
Hyperkalemia Management
Changes are listed in the classic, textbook description
However, patient's EKG findings often fail to follow the typical pattern
Initial
T Wave
s peaked or Tented (increased amplitude) in V2, V3, II, III
Next
ST depression
First degree
AV Block
(
PR Interval
increases)
QT Interval
shortening
Next (ominous harbinger)
QRS Duration
widening (>110 msec)
Loss of
P Wave
(
Junctional Rhythm
)
Sine Wave appearance
New
Bundle Branch Block
Final
Biphasic wave (sine wave) QRS and T fusion
Severe
Bradycardia
Imminent
Asystole
,
Ventricular Tachycardia
or
Ventricular Fibrillation
Changes exacerbated by
Hyponatremia
Hypocalcemia
Metabolic Acidosis
Hypermagnesemia
Chronic Renal Failure
with frequent, recurrent Hyperkalemia
Change from normal EKG to
Cardiac Arrest
may be rapid in these patients
Evaluation
Non-Renal Causes (transcellular shift,
Potassium
load,
Pseudohyperkalemia
)
Serious signs of Hyperkalemia present (EKG, symptoms)
Urgent
Hyperkalemia Management
Consider
Pseudohyperkalemia
Consider confirmatory testing (re-draw sample)
Consider exogenous source or transcellular shift
See
Hyperkalemia Causes
Eliminate causative factors
Evaluation
Decreased renal excetion
Urine Sodium
<25 mEq/L suggests decreased distal renal flow
See
Hyperkalemia Causes
Acute Kidney Injury
or
Chronic Kidney Disease
Congestive Heart Failure
Cirrhosis
Urine Sodium
>25 mEq/L with normal serum
Aldosterone
Primary tubular defects (e.g. RTA-4)
Obstructive uropathy
Tubular unresponsiveness to
Aldosterone
(e.g. SLE,
Multiple Myeloma
,
Sickle Cell Anemia
)
Medications (e.g.
Potassium
sparing
Diuretic
s,
Lithium
, Trimethoprim)
Urine Sodium
>25 mEq/L with low serum
Aldosterone
and normal serum renin
Primary
Adrenal Insufficiency
Medications (
Heparin
,
Cyclosporine
,
ACE Inhibitor
, ARB)
Urine Sodium
>25 mEq/L with low serum
Aldosterone
and low serum renin
Hyperglycemia
Primary renal tubular defects
Medications (e.g.
NSAID
s,
Beta Blocker
s)
Management
See
Hyperkalemia Management
References
Gibbs in Marx (2002) Rosen's Emerg Med, p. 1730-1
Klahr (2001) in Noble (2001) Primary Care p. 1359-62
Kim (2023) Am Fam Physician 107(1): 59-70 [PubMed]
Viera (2015) Am Fam Physician 92(6): 487-95 [PubMed]
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