Hyperkalemia & Hypokalemia

Glen E. Hastings MD
April 27, 1999

I. Physiology:

A.. Potassiums Role in Cellular Function
1,2,3
:
The normal plasma K
+
range is 3.5-5.0 mEq/L. The normal intracellular range is150 mEq/L. The
extracellular to intracellular ratio of 36:1 to 37.5:1 is maintained by a cell-membrane-bound
Na
+
/K
+
/ATPase pump, which uses energy from ATP to repetitiously extrude 3 Na
+
ions in exchange for
2 K
+
ions. This creates a negative (-75mV) charge across the resting membranes of the cells of the
body. Outward diffusion of K
+
ions through selective K
+
channels increases the negative electrical
potential further until at about 90mV the membrane depolarizes. This process drives nerve & muscle
conduction, hormone release, protein synthesis, embryogenesis, and many other bodily processes.
Hence the first symptoms of K
+
abnormalities are frequently muscle weakness or cardiac dysrhythmias.

B. Regulation of Potassium
1,2,3
:
Ingested K
+
is initially buffered intracellularly. Insulin, catecholamine levels & extracellular
pH influence cellular uptake & therefore determine extracellular K
+
levels. The major mode of K
+

regulation is through K
+
excretion by the principal cells of the cortical collecting duct of the kidney.
Na
+
/K
+
/ATPase pump structures are imbedded in the principle cells basement membrane adjacent to
the peritubular capillary. On the luminal surface of the principal cell are K
+
conductance channels, Na
+

conductance channels, a Na
+
/H
+
ion exchanger, & a K
+
/Cl
-
cotransporter. Potassium exits the luminal
surface because of a favorable concentration gradient, powered by the inward Na
+
flow through the Na
+

conductance channels, attracted by the Na
+
/K
+
/ATPase pump. Potassium secretion is thus dependent
upon the availability of luminal Na
+
, low urinary K
+
concentrations & low urine osmolality. It is therefore
related to luminal flow rates & to GFR. Anything that influences the Na
+
/K
+
/ATPase pump (e.g.
aldosterone), the Na
+
conductance channels (e.g. triamterine, & amiloride), the K
+
conductance
channels (opened by aldosterone signaling) or the K
+
/Cl
-
cotransporter (e.g. luminal Cl
-
concentration)
will effect K
+
excretion.

C. The Influence of the GI Tract in Potassium Balance
1
:
In a normal person, 92% of the potassium ingested is excreted by the kidney; 8% by the GI tract. GI
excretion may increase to 30% in CRF. It may also increase dramatically with diarrhea (Table 2).

D. The Transtubular Potassium Gradient (TTKG):
The TTKG measures the gradient across the cellular membrane of the principal cells in the cortical
collecting duct. In hypokalemia a TTKG <2 means that the cause is non-renal. In a hyperkalemic
patient, a TTKG >10 means that the cause is non-renal. The formula for TTKG:

Osm Urine
TTKG = K
+
Urine Osm Plasma
K
+
Plasma

II. Hyperkalemia:
A. Definitions
1,2
:
Hyperkalemia is defined as any plasma K
+
level greater than 5.0mEq/dL.
Severe hypokalemia requiring urgent treatment & EKG monitoring is when K
+
levels > 6.0mEq/dL.
Potentially life threatening levels are > 6.5mEq/dL.

B. Symptoms & Signs
1,2,4
:
Musculoskeletal weakness is typically the earliest symptom of hyperkalemia. Since hyperkalemia
lowers the depolarization threshold, part of the muscle tissue remains partially depolarized. Although
this can lead to muscle paralysis, serious cardiac dysrhythmias usually supervene before this occurs.
Sustained partial depolarization progressively flattens the P wave of the EKG & widens the QRS
complex. Ventricular repolarization however, is enhanced, so the T waves become peaked. With
progression these changes merge to form a sign wave pattern. Unfortunately, EKG changes are not
sensitive indicators of the danger of asystole, or ventricular fibrillation, so treatment decisions should be
based on laboratory determined measurements of plasma K
+
.
Hyperkalemia/Hypokalemia - Page 2

C. Causes of Apparent Hyperkalemia
1,2,3,4

Pseudohyperkalemial
1,3
: Laboratory Error, Hemolysis & K
+
Leak:
Mechanical trauma, clenching & unclenching of the hand, & allowing unspun blood samples to sit are all
causes of hemolysis. These as well as simple laboratory error cause falsely elevated K
+
levels.
Pseudohyperkalemia may also occur with marked thrombocytosis (>400,000), or leukocytosis
(100,000). It is first necessary to exclude these possibilities before proceeding with treatment.

D. Causes of True Hyperkalemia: Hyperkalemia is the result of an increase in K
+
intake, a decrease in
K
+
excretion or a shift of potassium from the intracellular to the extracellular compartment.

True Hyperkalemia: Drugs:
Excluding patients with frank renal failure, most cases of hyperkalemia are of multifactorial origin, not
infrequently involving a prescription drug, coupled with age or disease related impairment of GFR, Renal
excretion of K
+
is decreased when GFR<25% of normal). A list if drugs most frequently implicated
along with their modes of action is shown as Table 1.

Table 1: K
+
Altering Drugs & Their Mechanisms of Action
2,4
Type of Drug Drug Mechanism of Action
Diet & Dietary Supplement
Potassium Supplements
Salt Substitutes
Exogenous K
+
Exogenous K
+

K Sparing Diuretics
Spironolactone
Amiloride
Triamterine
Aldosterone Antagonism
Na
+
channel blockade in principal cells
Na
+
channel blockade in principal cells
Angiotensin II Blockers
ACE Inhibitors
AT II Receptor Blockers
Aldosterone, RBF & GFR.
Aldosterone, RBF & GFR.
Antiinflammatories NSAIDS Renin, Aldosterone, RBF & GFR.
Adrenergic Drugs
-Blocking Agents
-Adrenergic Agonists
Impaired Cellular Glucose Uptake
Impaired Cellular Glucose Uptake
Antibiotics
Trimethoprim
Potassium Penicillin G
Pentamidine
Na
+
channel blockade in principal cells
Exogenous K
+
Na
+
channel blockade in principal cells
Immune Modulating Drugs
Cyclosporine
Tacrolimus
Aldosterone Release, & Na
+
/ K
+
ATPase Activity
Aldosterone Release, & Na
+
/ K
+
ATPase Activity
Miscellaneous
Succinylcholine
Digoxin
Heparin
K
+
channel blockade in principal cells
Na
+
/ K
+
ATPase Activity
Aldosterone Synthesis

True Hyperkalemia Secondary to Decreased Excretion
1
: Prerenal Azotemia:
In congestive heart failure, liver failure with ascites, & chronic renal disease with volume depletion, a
state of ineffective circulating blood volume occurs where insufficient Na is delivered to the cortical
collecting duct for K
+
secretion to occur. Hyperkalemia is likely when urine output < 600cc/day.

True Hyperkalemia Secondary to Decreased Excretion
1
: Kidney Failure:
Hyperkalemia does not occur in chronic renal failure until the GFR is < 10cc/minute, or in patients with
hypoaldosteronism or aldosterone resistance. It is common in acute renal failure caused by acute
tubular necrosis because of concomitant metabolic acidosis & K
+
release secondary to hemolysis or
tissue necrosis. Acute glomerulonephritis, sickle cell disease, interstitial nephritis, systemic lupus
erythematosus, amyloidosis, lead nephropathy, obstructive uropathy with associated type 4 RTA,
postrenal transplantation & pseudohypoaldosteronism may all produce hyperkalemia.

True Hyperkalemia Secondary to Decreased Excretion
1
: Hyporeninemic Hypoaldosteronism:
After drugs & kidney failure, the third most common cause of hypokalemia is hyporeninemic
hypoaldosteronism, a condition usually occurring in diabetic patients or those with chronic interstitial
nephritis & mild to moderate renal failure (GFR 20 60cc/minute). The condition is confirmed by the
Hyperkalemia/Hypokalemia - Page 3
presence of (usually asymptomatic) hyperkalemia, an inappropriately low urinary K
+
, a transtubular K
+

gradient (TTKG) < 5 & a low aldosterone level. Prescription of an NSAID to such a patient may
precipitate life threatening hyperkalemia. The condition is treated with low K
+
diet & loop or thiazide
diuretics combined with NaHCO3. Refractory cases may require fludrocortisone or Kayexalate

True Hyperkalemia Secondary to Decreased Excretion
1
: Adrenal Insufficiency or Resistance:
Autoimmune disease & HIV have supplanted tuberculosis & primary atrophy as causes of Addisons
disease. The most common form of congenital adrenal hyperplasia is 21-hydroxylase deficiency which
impairs glucocorticoid and mineralocorticoid synthesis which stimulating ACTH producing virilization,
salt wasting & hyperkalemia during infancy. It is treated with steroid replacement. Generalized
Pseudohypoaldosteronism results from a congenital diminution of aldosterone receptors. The acquired
form occurs as a result of tubulointerstitial dysfunction in such conditions as amyloidosis, chronic
pyelonephritis, or obstructive uropathy. Both feature salt wasting, hypovolemia, & hyperkalemia but
differ from adrenal insufficiency in that both renin & aldosterone are increased.

True Hyperkalemia 2
o
to Decreased K
+
Excretion
1
: Distal Hyperkalemic Renal Tubular Acidosis:
In distal hyperkalemic (Type 4) RTA K
+
& H
+
ion excretion are both impaired producing a hyperchloremic
acidosis with hyperkalemia. The most common intermediate causes are insufficient aldosterone
production or aldosterone resistance. Obstructive uropathy & sickle cell disease are common causes.
Management is as with hyporeninemic hypoaldosteronism.

True Hyperkalemia 2
o
to Decreased K
+
Excretion
1
: Selective Renal Tubular Defects:
Gordons syndrome features hyperkalemia, & volume expansion with related hypertension, in patients
with normal renal function. It results from a selective increase in the tubular reabsorption of Cl which
expands circulating volume depressing renin & aldosterone. Treatment with thiazides. Selective
defects in K are seen in cyclosporine nephropathy, & lupus nephritis.

True Hyperkalemia 2
o
to Increased K
+
Intake or Release
1
: Tissue Injury & Hemolysis:
Rapid tumor lysis during chemotherapy, rapidly progressing hemolytic anemias, crush injuries,
rhabdomyolysis secondary to heat injury, neuroleptic malignant syndrome, or drugs, transfusion
reactions or stored blood administration may produce hyperkalemia. Vigorous physical exercise alone
may cause hyperkalemia as do the drugs & supplements in Table 1.

True Hyperkalemia 2
o
to Intracellular/Extracellular K
+
Shifts
1
: Metabolic Acidosis & Hypertonicity:
Respiratory acidosis does not produce hyperkalemia because the excessive H
+
ions and their
accompanying anions are distributed to both the intracellular & extracellular compartments & do not
therefore cause a K shift. Metabolic acidosis caused by inorganic acids and conditions like diabetic
ketoacidosis featuring hypertonicity are frequent causes of hyperkalemia, best treated by remedying the
precipitating condition.

Hyperkalemia 2
o
to Intracellular/Extracellular K
+
Shifts
1
: Familial Hyperkalemic Periodic Paralysis:
Familial hyperkalemic periodic paralysis is an autosomal dominant inherited condition, caused by
dysfunction of the sodium channels of the muscles of the limbs resulting in periodic episodes of
weakness accompanied by mild hyperkalemia which may be precipitated by cold, exercise, or K
+

loading. It may be diagnosed by family history & treated with a high CHO diet. Acetazolamide; &
albuterol may be used during acute attacks.
E. Diagnosis:
A history of drugs and medications, family history, dietary habits and concomitant illnesses is
essential.
Physical exam should focus upon the blood pressure, postural change in blood pressure & pulse, &
signs of congestive heart failure, liver failure with ascites, or acute or chronic renal disease.
Initial laboratory values should include serum & urine electrolytes & osmolality, BUN & creatinine,
arterial blood gasses, routine urine analysis, liver profile, & EKG. Renin & aldosterone levels,
cosyntropin stimulation, echocardiography, & chest x-ray may also be useful in specific cases..
F.Emergency Treatment of Acute Hyperkalemia
1,2,3
:
Hyperkalemia/Hypokalemia - Page 4
Correction of plasma K levels above 6.0-6.5 mEq/dL or with EKG changes should generally by
performed under continuous EKG monitoring. In previous years NaHCO3was included in most protocols
for treatment of hyperkalemia. Recent experience however has shown NaHCO3 to be unreliable unless
the underlying problem is metabolic acidosis caused by an inorganic agent. The agents of choice &
dosages are shown in Table 2
1,2,3
below:
Therapy & Mechanism of Action Dosage Onset Duration of
Effect
Antagonism of membrane effects of
hyperkalemia
Calcium Gluconate (10%)
10-30 mL, IV < 5 minutes 60 minutes
Stimulation of potassium uptake into cells
Glucose and insulin


Inhaled Albuterol

10-20U regular insulin
with 30-50 grams glucose
over 15-30 minutes
10-20mg

30 minutes


30 minutes

3-6 hours


2 hours
Removal of potassium from the body
Diuretics (furosemide)
Cation-exchange resin

Peritoneal dialysis or hemodialysis

40 mg, IV
20-40 g rectally or orally
with sorbitol
N/A

Starts with
diuresis
60 minutes
120 minutes
A few minutes

Variable
6 hours

Variable

III. Hypokalemia
1,3,5
:

A. Definitions
Mild Hypokalemia: 3.0-3.5 mEq/L=Total body deficit =150-300 mEq/1.75m
2

Moderate Hypokalemia: 2.5-3.5 mEq/L=Total body deficit =300-500 mEq/1.75m
2

Severe Hypokalemia: <2.5 mEq/L=Total body deficit =>500 mEq/1.75m
2


B. Symptoms of Hypokalemia
1
:
Mild hypokalemia is most often asymptomatic. As plasma levels drop below 3.0mEq/dL nonspecific
symptoms like weakness, malaise & constipation appear. At levels less than 2.5mEq/dL, hypotension
& rhabdomyolysis secondary to decreased glycogen synthesis may occur. Below 2.0mEq/dL
interstitial nephritis or an ascending paralysis may appear. Hypokalemia & cardiac arrhythmias
increase, especially in the presence of ischemia, hypertension or digitalis therapy.

C.Causes of Hypokalemia
1,3,5
:
The most common cause of hypokalemia is excessive renal loss or an intracellular shift of extracellular
potassium induced by prescription drugs. Less frequently hypokalemia results from a shift of K
+
into
the intracellular compartment induced by metabolic alkalosis, from inadequate potassium intake, from
excessive loss in diarrheic stool, or from another cause of renal wasting.



Hypokalemia Secondary to Drugs
1,3,5
:
Drugs may precipitate hypokalemia in one of three ways: by causing an intracellular shift of potassium,
by accelerating renal loss, or by causing diarrhea. Drugs commonly causing hypokalemia are listed in
Table 3:

Table 3: Drugs Causing Hypokalemia & Their Mechanisms of Action
5
Drugs Causing Intracellular K
+
Shift Drugs that Renal K
+
Loss Drugs that Fecal K
+
Loss
Adrenergic Agonists
Epinephrine
Decongestants
Bronchodilators
Tocolytic Drugs
Diuretics:
Thiazides
Loop Diuretics
Steroids & Steroid-like Drugs
Fludrocortisone
Phenolphthalein
Na Polystyrene Sulfonate
Hyperkalemia/Hypokalemia - Page 5
Xanthine Derivatives
Theophylline
Caffeine
Overdose Related Hypokalemics
Insulin
Verapamil
Chloroquine
Barium
Toluene
Hi dose glucocorticoids
Licorice
Gossypol (an herbal remedy)
High dose Penicillins
Magnesium Depleting Drugs with 2
o
K
+
:
Cisplatin
Foscarnet
Amphotericin D
Aminoglycosides

Hypokalemia Secondary to Inadequate Intake or Malabsorption of K
+1
:
Especially likely to develop hypokalemia along with potentially life threatening hypophosphatemia are
patients with anorexia nervosa, or other starvation syndromes, chronic binge alcoholics who do not eat
during binges, and persons who practice geophagia. Geophagia, the ingestion of clay from the soil
binds K
+
in the gut & prevents absorption,

Hypokalemia Secondary to Gastrointestinal Loss of K
+
:
In addition to the bowel stimulating drugs shown in Table 3, vomiting, acute or chronic secretory
diarrhea, or congenital diarrhea, may cause hypokalemia. Vomiting induces metabolic alkalosis 2
O
to
Cl
-
loss. Renal K
+
wasting 2
O
to HCO3
-
loss ensues. Table 4 lists other sources of g. i. K
+
loss:
Table 4: Causes of Gastrointestinal K
+
Loss
5,1
Infectious Diarrhea
Cholera
Salmonella
Strongyloides
Yersinia
AIDS related diarrhea
Tumors
VIPoma
Villous Adenoma of Colon
Zollinger-Ellison Syndrome
Cancer Therapy
Chemotherapy
Radiation Enteropathy
Jejunoileal bypass
Enteric Fistula
Malabsorption Syndromes
Congenital Chloride Diarrhea
Vomiting & Nasogastric tube
drainage: Cause loss of chloride
& metabolic alkalosis
producing renal K
+
loss.

Hypokalemia Secondary to Increased Intracellular uptake of K
+1
:
Two common conditions featuring hypokalemia 2 to intracellular shifts are during the correction of DKA,
& in delirium tremens. In DKA the shift is induced by insulin. In DTs by epinephrine. Severe
hypothermia may produce an intracellular K
+
shift with significant hypokalemia. Hyperthyroidism
presents in Asian & Hispanic men with hypokalemia & weakness about 9% of the time. Increased
blood cell production in hypermetabolic states such as acute myelogenous leukemia, or newly treated
megaloblastic anemia is another. Familial Hypokalemic Periodic Paralysis is an inherited disorder of
the muscle cell calcium channels causing hypokalemia & profound (usually distal) muscular weakness.
Onset is before age 25. Attacks usually occur at rest & may be precipitated by carbohydrate loading.
Treatment is with acetazolamide & low carbohydrate diet.
Hypokalemia Secondary to Accelerated Renal K
+
Loss Related to Renal Tubular Defects
1,3,5
:
The most frequent cause of excess renal K
+
loss is metabolic alkalosis following Cl
-
loss 2
o
to vomiting.
Less frequent causes include the metabolic alkaloses 2
o
to various endocrinopathies which will be
described in the next section and the renal tubular defects discussed below:
- Renal tubular acidosis (RTA): In RTA Type I (Classic distal RTA) distal H
+
secretion is impaired,
increasing Na
+
reabsorption & K
+
excretion. Acidification of the urine usually controls the
hypokalemia. In proximal (Type II) RTA, increased HCO3
-
& Na
+
are delivered to the distal renal
tubule causing hypokalemia. Treatment requires both HCO3
-
& K
+
supplementation.
- Liddle's syndrome is a rare autosomal dominant condition in which enhanced sodium channel
activity increases distal Na
+
resorption & thereby produces hypokalemia & hypervolemia related
hypertension. Amiloride or triamterine but not spironolactone are effective treatments.
- The Syndrome of Apparent Mineralocorticoid Excess results from an impairment of cortisol
metabolism in the cortical collecting ducts which produces manifestations similar to Liddles
Syndrome. The difference is that exogenous corticosteroids correct the defect. Amiloride, or
spironolactone & Na restricted diet will correct the hypokalemia.
- Bartter's syndrome is an autosomal recessive condition which usually presents in childhood as
Hyperkalemia/Hypokalemia - Page 6
growth retardation, hypokalemia, metabolic alkalosis, hyperaldosteronism & hyperreninemia. The
defect is increased Na
+
resorption in the thick ascending loop of Henle. Management includes K &
Mg replacement, NSAIDS, & amiloride or triamterine.
- Gitelmans Syndrome is also called the syndrome of hypomagnesemia-hypokalemia with
hypocalciuria. It is caused by an abnormality in the NaCl cotransporter in the distal convoluted
tubule. Its effects are milder than in Bartters Syndrome & may present in adults

Hypokalemia Secondary to Accelerated K
+
Loss Secondary to Endocrinopathies
1,3,5
:
Less frequent causes of hypokalemia include the metabolic alkaloses 2
o
to various endocrinopathies:
- Primary Hyperaldosteronism (Conns Syndrome), 60% of which is caused by an
secreting adenoma of the adrenal cortex, & 40% by hyperplasia, presents with hypertension, &
hypokalemia. Adenomas are treated surgically while hyperplasia is managed with amiloride,
spironolactone, ACE inhibitors, or calcium channel blockers.
- Glucocorticoid Remediable Hyperaldosteronism is a rare autosomal dominant disorder
occurring before age 21, in which aldosterone production occurs in the wrong layer of the adrenal
cortex making it subject to over-stimulation by ACTH. Its management involves administering
glucocorticoids which suppress ACTH production.
- Congenital Adrenal Hyperplasia may be caused by one of two inherited enzyme deficiencies.
11-hydroxylase deficiency causes hypertension, hypokalemia, & virilization. 17-hydroxylase
deficiency causes only hypertension & hypokalemia but not virilization. Both occur in childhood.
- Cushings Syndrome whether of adrenal or pituitary origin may cause hypokalemia & metabolic
alkalosis. Treatment depends upon the cause.
- Hyperthyroidism may present with hypokalemia & weakness in 2% to 8% of Asian & Hispanic
men. It responds to exogenous K
+
, but may cause rebound hyperkalemia. Hypokalemia may
occur episodically & be thereby confused with familial hypokalemic periodic paralysis.

D. Diagnosis of Hypokalemia
1,3,5,7

There are many diagnostic decision trees for hyponatremia. The one selected & shown on the next
page is based employs readily available clinical information. It excludes hyponatremia secondary to
acute conditions such as acute tubular necrosis, & the metabolic acidoses associated with ethylene
glycol or methanol ingestion. It also excludes hyperthyroidism familial hypokalemic periodic paralysis &
other conditions causing transient intracellular shifts of potassium.
Hyperkalemia/Hypokalemia - Page 7
Chronic Hypokalemia

Exclude
Pseudohypokalemia


Exclude Drugs



or Normal Blood
Pressure

Blood Pressure



Urine K
+

<25mMol/L

Urine K
+
>25mMol/L

Renin:



Renin:
Malignant
HBP
Renin
secreting
tumor



HCO3:
Previous
use
of diuretics.

Aldosterone:
Cushings
Liddles
Licorice
or
Normal
HCO3:
HCO3
losing
Diarrhea
K
+
Intake
HCO3:
RTA I or
II
DKA
Delerium
Tremins.
Aldosterone:
1
o

Hyperaldosteronism
Glucocorticoid
Responsive

Hypoaldosteronism






HCO3:
Vomiting or NG loss
Current Diuretic Use
Bartters Syndrome
Gitlemans Syndrome
Cl Losing Diarrhea
or
other Cl depletion.
Post Hypercapnia






E. Treatment of Hypokalemia
1
How Much Is the Deficit?:
In general a reduction in K from 4mEq/dL to 3mEq/dL represents loss of 200 to 400mEq of total body
potassium. This estimate does not include transcellular shifts.
Diet, Supplements & Salt Substitutes
1,5
:
As with many things on medical practice, the best way to treat hypokalemia is to prevent its
occurrence in the first place, & the safest way to prevent its occurrence is through diet & oral
supplements. Table 5 is a list of foods high in K
+
content.
Table 5: High K
+
Foods
Highest (>1000mg/100g):
Dried Figs
Molasses
Seaweed
Very High (>500mg/100g):
Dried Fruits (Dates, Prunes)
Nuts
Avocados
Bran Cereals
Wheat Germ
Lima Beans
High Content (>250mg/100g):
Vegetables:
- Spinach
- Tomatoes
- Broccoli
- Winter Squash
- Beets
- Carrots
- Cauliflower
- Potatoes
High Content (>250mg/100g):
Fruits:
- Bananas
- Cantaloupe
- Kiwis
- Oranges
- Mangos
Meats:
- Beef & Veal
- Pork
- Lamb

Unfortunately dietary K
+
alone will not correct the K
+
depletion caused by diuretics because dietary K
+

is almost completely coupled with phosphates. The physiological basis for diuretic induced K
+

depletion is metabolic alkalosis secondary to Cl
-
depletion, so supplementation with KCl is also
required, either in the form of supplements or salt substitutes. Unfortunately, these substances are
the most frequent sources of inadvertent hyperkalemia. Salt substitutes are known to cause small
bowel perforation in rare instances. This is least likely when micronized forms are used.

Hyperkalemia/Hypokalemia - Page 8
Magnesium depletion will prevent effective K
+
replacement, & may need to be replaced concomitantly.
Spironolactone mitigates both K
+
& magnesium loss & may be more appropriate for those with
cardiovascular risk factors. Spironolactone works by inhibiting the binding of spironolactone to its
receptor, while both triamterine & amiloride are independent of aldosterone.
Intravenous K
+1,3
:
Patients with cardiovascular emergencies secondary to hypokalemia related cardiac arrythmias should
be admitted to the CCU for K
+
replacement under continuous EKG monitoring. KCl should Never be
injected directly into the vein as the body has no mechanism for protecting itself from sudden surges of
K
+
. In true emergency situations, infusion rates up to 20 or even 40mEq/hour for short periods of time
may be used in order to terminate life-threatening arrhythmia. To achieve such flow rates 100 up to
400mEq of KCl might be mixed with 1000cc of saline. Thereafter the flow rate should be reduced to a
more conventional rate.
Under ordinary circumstances KCl concentrations should not exceed 60mEq in each 1000cc of IV fl uid.
Under ordinary circumstances KCl replacement rates should not exceed 20mEq/hour even with
monitoring.

As with oral supplementation, magnesium deficit may prevent K
+
replacement & should be replaced
concomitantly.

In patients with metabolic alkalosis (as in diuretic or vomiting induced hypokalemia) there is a
simultaneous Cl
-
deficit, so Cl
-
must be replaced along with K
+
.

In the treatment of diabetic ketoacidosis there frequently develops a PO4 deficit, so correction with a
combination of KCl & KPO4 may be warranted. In other forms of metabolic acidosis KHCO3 is the
preferred replacement therapy because Cl
-
is limited to the extracellular compartment, while HCO3.is
not. This means that the infused K
+
will also remain longer in the extracellular compartment &
correction of the total body deficit will be delayed
1
.

IV. References:

1. Peterson LN, Levi M: Disorders of potassium metabolism, Chapter 5 in Schrier, RW (ed): Renal &
Electrolyte Disorders, 5
th
Edition. Philadelphia, New York, Lippencott-Raven, 1997, pp 192-240.

2.Perazella MA, Mahnensmith RL. Hyperkalemia in the elderly J Gen Intern Med 1997;12:646-656.

3.Mandel AK. Hypokalemia & hyperkalemia. Med Clin N Amer 1997;81(3):611-639.

4.Greenberg A. Hyperkalemia: Treatment options. Semin in Nephrolol 1998;18(1):46-57.

5.Gennari FJ. Hypokalemia. N Engl J Med 1998;339(7):451-8.

6.Halperin ML, Kamil KS Potassium. Lancet 1998;352:135-40.

7.Levinsky NG: Fluids and Electrolytes, in Petersdorf RG, Adams RD, Braunwald E, Isselbacher KJ, Martin
JB, Wilson JD (eds): Harrison's Principles of Internal Medicine (12 ed.). New York, McGraw-Hill Book
Co, 1991, pp. 278-289.