Disorders of Potassium Metabolism

Potassium is one of the major ions in the body, with one
Total body ranging storage at about 3500
mEq, being distributed predominantly in the intracellular space (over 98%). There are an estimated 40 to 50
mmol / kg body weight in the intracellular fluid (LIC) and about 1 mmol / kg body weight in the extracellular fluid (ECF). The
Potassium main function lies in the generation of potential
rest of the cell membrane, with the importance of this
means for the maintenance of biological functions. The
alterations in plasma concentration of K + bring as
result in significant changes in the excitability characteristics of nervous tissue, heart and skeletal muscles and smooth
Ticos.
The major reservoirs are potassium and skeletal muscle
liver. Less than 2% of potassium is in the LEC, being this the only measurable fraction in clinical practice
daily. Serum potassium levels at any given time will be
the result of a delicate and complex balance, whereas
know to understand the pathophysiologic processes that may
be involved when it is altered.
Potassium balance
To understand the metabolism of K +, we must distinguish two
different processes, the external balance (between the environment and
the internal environment) and internal balance (between compartments
intracellular and extracellular) of the electrolyte. Normally the
body regulates its external balance by entering that
is given by the diet (containing K + ranging in
Normally, between 40 and 120 mEq / d) and the therapeutic input, both intravenous and enteral and egress, represented mainly by renal clearance, since only
between 5 and 10 mEq per day are lost in stool, while
eliminating the sweat less than 10 mEq / d.
A varied diet containing about 1 mmol Western /
Kg / day of potassium, of which 90% is absorbed in the digestive tract.
Normally this same percentage of potassium can be removed by the distal nephron, with consideration of losses
Faecal only in cases of renal or severe diarrhea.
As for the internal balance, redistribution of potassium between
intra and extracellular compartments is the acute form
regulation largest. The intracellular concentration of potassium is about 150 mEq / L, while in the
extracellular fluid may range between 3.5 and 5.5 mEq / L. This chemical gradient is generated and sustained by a process basically
active transcellular ion transport with energy
(The Na + / K + ATPase, with active transport of three sodium ions
the income of 2 extracellular and the intracellular potassium ions) and a
passive process (the output of potassium into the LEC is provided by the
chemical gradient and the permeability of the cell membrane).
Potassium redistribution between intracellular and extracellular compartments depend on changes in membrane potential,
variations in the acid-base status and the presence of solutes
osmotically active in the LEC, which potassium moves in different directions. Considering the above, the agents
stimulate the Na / K ATPase determined entry
potassium intracellular space (eg  2 adrenergic and insulin).
Metabolic acidosis increases potassium outer passage
and alkalosis cell tends to produce the opposite effect (through
intracellular K + exchange with protons of the LEC). Calculated
For every drop of pH 0.1 of plasma concentration
increases K + 0.6 mEq / L, and drops the same amount when the pH rises, this ratio should be used as guidance only, as the final value of hyperkalemia depends on many
other factors, primarily renal excretion: so much so that
many metabolic acidosis usually present with K + depletion. The
hyperosmolarity of LEC (eg.: severe hyperglycemia) occurs
the extracellular passage of water, with passive drag to said K +
compartment and can lead to hyperkalemia.
Regulating potassium excretion is renal basically,
taking place in the cortical collecting duct (TCC). There comes only
10% of K + filtrate, since the remaining 90% has been absorbed in
anterior segments. Removal of potassium depend
the presence of a greater or lesser number of negative charges in the
TCC lumen, which depend on sodium reabsorption from the
presence of a greater or lesser amount of chlorine or hydrogen and
urine volume reaching the TCC (a larger volume of urine,
greater the potassium moves to achieve electrochemical balance on both sides of the tubular membrane). In the regular tion of K + excretion by the TCC, aldosterone plays
a key role, increasing the secretion of K + in
the same. Likewise, increases aldosterone secretion
after a load of potassium (very discrete elevations,
from 0.1 to 0.2 mEq / L of K + in the plasma produces a significant increase in the release of aldosterone), while
reducing the ion depletion. Aldosterone acts
encouraging all processes secrete K +: increases
the number of open channels of Na + / K + on the membrane
luminal and increases the activity of the Na + / K + ATPase
in the basolateral membrane. Atrial natriuretic peptide
acts somewhat opposite way, since it inhibits
Na + reabsorption by decreasing the number of channels
Na + open, thus reducing the negative charges in the light
TCC and therefore hindering the removal of K +.
In addition to these physiological mechanisms influencing directly or indirectly in the urinary excretion of K +, there
other factors to consider when analyzing the
potassium metabolism in a given patient. By
eg
Loop diuretics and thiazides, through its various
sites of action, determine that the TCC reaches as many solutes (mainly Na + and Cl-), more
favoring water drag urinary K + loss.
The acidosis stimulates secretion of K + distal and alkalosis
acts in reverse.
Potassium-sparing diuretics act closing
Na channels, Amiloride and triamterene directly, and
aldosterone competing with spironolactone.
Whole situation conducive sodium retention in
plasma will result in increased reabsorption
tubular Na +, K + with distal secretion increased. These situations occur by the effect of aldosterone and
glucocorticoids.
ADH stimulates K + secretion by increasing
the number of specific K + channels and empower
aldosterone.
Finally, remember that the magnesiuria is
another factor causing renal potassium loss, unknown physiological reason for this phenomenon.
Hypokalemia
Defined with plasma K + <3 .5="" l="" meq="" p="">but symptoms usually appear when the concentration
is <3 .0="" and="" cardiac="" l="" manifestations.="" meq="" muscle="" p="" predominantly="">Some classify it as mild (between 3.5-3 mEq / L), moderate
(3-2.5 mEq / L) and severe (less than 2.5 mEq / L)
CLASSIFICATION
It is of clinical and therapeutic importance define the mechanism
responsible pathophysiological hypokalemia, since a
rational treatment should be aimed at correcting this
alteration. To this end, we can divide the causes of hypokalemia in three main groups: renal losses, losses
extrarenal compartment and redistribution between intra and
extracellular. In turn, these 3 groups can be subdivided,
by acid-base disorders associated as detailed
in Table 1.
CLINIC
Symptoms are usually mild and nonspecific:
1-muscular symptoms:
Muscle Cardiac arrhythmias (enhanced with digital)
Musculoskeletal: fatigue, restless leg syndrome,
muscle weakness (a predominance of lower limbs), cramps, decreased strength, diaphragmatic weakness, rhabdomyolysis
in cases of severe depletion.
Smooth muscle: constipation, ileus, gastric atony
2-Renal: There may be a decreased ability to concentrate urine
onset of a state of nephrogenic diabetes insipidus, with
decreased sensitivity of the distal tubule of action
ADH, and in case of chronic hypokalemia, can be reached
to produce tubular cell vacuolation. It manifests
with polyuria and polydipsia, and can be found in the sediment
Urinary albuminuria, hyaline or granular. K + depletion stimulates production of ammonium, renin and
prostaglandins, leading to medullary interstitial disease.
3-neurological symptoms: paresthesias and decreased
or abolition of tendon reflexes.
4-ECG Changes: Changes not saved correlate with the intensity of the disorder, hypokalemia favors the appearance of various types of arrhythmias (both atrial and ventricular), especially in patients with
Using digital. ECG should be performed control in all patients with serum K + <3 flattening="" l.="" meq="" often="" p="" the="">or T wave inversion, appearance of prominent U waves
and ST segment depression.
Approach to the Patient with hypokalemia
1) Complete physical exam: assess symptoms generated by hypokalemia, blood volume, clinical condition passes through the patient and medication that receives or has received
(Eg high-dose diuretics in the run).
2) Evaluate the entry of K +: hypokalemia rarely
is due to low intake of potassium, since if swallowed
kidney bit retains the ability to excrete not depleted in the same subjects. However, a poor diet
in K + and high losses will manifest itself as depletion
severe. In patients with marked anabolism (recovery
ketoacidosis or nutritional supplement in malnourished), the
gain intracellular anions (RNA, phosphates) will cause the entry of intracellular potassium.
3) Check extrarenal losses: Vomiting
themselves are not considered to cause loss of K +, since
low content having gastric fluid (<15 l="" meq="" p="">Vomiting and nasogastric suction generated gain
bicarbonate, with metabolic alkalosis and aldosterone stimulation by volume depletion, which leads to increased supply
bicarbonate to TCC and kaliurética action of aldosterone. Diarrhea is considered another cause of loss, given the high
content of K + handling the colon (search coexistence
metabolic acidosis). Should also be considered as profuse sweating probable site of losses, although
an unusual cause.
4) Evaluate the conditions that promote
intracellular potassium shift: bronchodilators, insulin, adrenergic states such as hypotension,
stress, hypoglycemia, exercise or delirium tremens.
5) plasma electrolytes: It serves not only to quantify the magnitude of hypokalemia, but also for
the status of sodium, chlorine and HCO3-, determining
internal environment and associated disorders: contraction
volume, hyponatremia, metabolic alkalosis, etc..
6) acid-base status: in case of metabolic alkalosis
etiology should be sought and corrected, since it generates and
perpetuates hypokalemia. Remember that often causes respiratory alkalosis no major changes in serum potassium.
7) urinary electrolytes: Not only is useful in assessing
renal losses of K +, but also to assess the
Na + and Cl-: for example, high levels of Na + and Cl-in urine
could indicate either diuretic action, if not
receiving it, we will probably face a Bartter syndrome. The first approach is to quantify the loss of K +. In general terms, a
daily excretion of greater than 25 K + mEq / d, in a patient
with hypokalemia, should suggest a component
renal involved therein.
They must know daily urine volume and osmotic diuresis rule. The urinary concentration of K + is a variable that can easily be altered by reabsorption
water level TCC, which is used for a determination that serves to quantify the loss of K + Renal
transtubular gradient K +.
8) transtubular potassium gradient (GTTK)
 U / P K +
 GTTK + =
 U / P osm
The GTTK would be a way to "correct" the secretion of potassium
distal to water absorption. Example: if the TCC exists
concentration of 10 mEq / l K + and no absorption occurs
water, K + concentration in urine is 10 mEq / L;
but if absorbed 0.75 L of water, the urinary
reach 40 mEq / L and urine osmolality will also
greater. This occurs simply by water absorption without
mediate change in the absolute quantity of K + ions.
That is why to consider GTTK required as
premise that urine osmolarity is greater than the
plasma (by which we ensure that truly
There reabsorption of water) and there is no osmotic diuresis;
otherwise it can not use this index. Remember
GTTK assumed that the arriving osmoles CBT are
potassium absorbed and that is not absorbed or excreted.
There is no exact number GTTK to diagnose any particular clinical situation, however, higher than 7 are highly indicative of the existence
hyperaldosteronism, above 4 suggests renal potassium loss and lower values ​​of 2 you could say that
TCC properly absorbed potassium that arrives there,
consistent with a situation of hypokalemia.
Whenever there are large renal K + losses should
the study to rule out direct hyperaldosteronism, bicarbonaturia and persistence of negative charges in the lumen
TCC.
Some considerations:
Bartter syndrome: we compare it with the intake
furosemide, because they contraction of patients with
volume, metabolic alkalosis, hypokalemia, and sodium chloride
and concomitant elevated urinary magnesium loss
calcium, and secondarily with hypertrophy Hiperreninism
juxtaglomerular apparatus. The cause is a genetic alteration
tica electroneutral transport of Na + / Cl-/ K + handle
Henle.
Gitelman syndrome: could compare to Action
of thiazides. The defect is a mutation in the cotransport
Na + / Cl-distal convoluted tubule, with losses
chlorine and sodium, volume depletion, hyperreninemia, hypo- hyperkalemia and hypomagnesemia. No urinary calcium loss.
Liddle syndrome: mutation that causes increased
absorption epithelial sodium channel permanently
open, which generates chlorine retention in the lumen and
negative potential. It manifests with hypertension hiporreninismo, absence of aldosterone, hypokalemia and alkalosis
metabolic.


CLINIC
Clinical manifestations are neuromuscular and heart, the latter being potentially fatal:
1 Neuromuscular symptoms: Weakness is what
most characteristic, predominantly of the lower limbs, rarely reaching ascending flaccid paralysis, also
can observe osteotendinous paresthesia and areflexia.
2-Cardiac arrhythmias: As you increase
serum K + values ​​are produced different alterations
electrocardiographic but since the rate of progression
each patient is unpredictable and there is variability in
serum levels that cause different changes, there
Consider that can appear at any time
ventricular arrhythmias. All changes are exacerbated
with hyponatremia, hypocalcemia and acidosis.
K + between 5.5-6.0 mEq / L: peaked T waves (most striking
precordial)
K + between 6.0-7.0 mEq / L: PR prolongation, lower voltage
of R, ST depression, QT prolongation and QRS widening
K + between 7.0-7.5 mEq / L: T wave flattening, loss
P wave (atrial asystole) and greater widening of
QRS
K +> 8.0 mEq / L: biphasic appearance of representing the
QRS fusion with T wave ANNOUNCES STOP
VENTRICULAR IMMINENT.
Approach to the Patient with hyperkalemia
Should be considered:
1) If life-threatening hyperkalemia. Perform ECG and assess neurological examination. If so
out will proceed immediately to treatment. The
and chronic forms that occur in young patients
are better tolerated. The presence of changes in the ECG
 use of blockers and the presence of cell lysis boxes
are elements that should alert us to rapidly changing
of K +.
2) If hyperkalemia is real: Discard causes
pseudo hyperkalemia (CBC). Evaluate status LEC
and BG value.
3) If the kidney correctly removes K +. First we must know the acid-base status and function
renal (urea, creatinine). It is expected that in cases of hyperkalemia daily excretion is> 200 mEq / day (a normal adult can excrete up to 450 mEq / day to an overload
potassium). This will depend on the concentration of K + urinary and urinary flow. If GTTK is <10 a="" in="" p="" patient="">with hyperkalemia, should be sought if aldosterone levels are abnormally low or if it is the TCC which
not responding to aldosterone. To this end, should be taken
samples for measurement of plasma renin and aldosterone
or they can make a therapeutic trial with 100 g
fludrocortisone. If in presence of the drug increases
the GTTK, will approach the diagnosis of mineralocorticoid deficiency, otherwise the likely defect
is tubular.
Other causes of low urine K + in the presence of hyperkalemia:
low distal sodium supply: for proper disposal
K + is required electrogenic sodium absorption. You can test with administration of diuretic.
Alteration in sodium channel luminal membrane
TCD: occurs by sparing diuretics and
high-dose trimethoprim.
Increased permeability to chloride: use of cyclosporin and
Gordon Syndrome (called "shunt chlorine" or pseudohypoaldosteronism type II)
4) Income potassium. The great contribution of potassium only
will cause to consider cases of patients with impaired renal function.
5) Existence of shift of K +: tissue necrosis, hyperchloremic metabolic acidosis, the antagosnismo  adrenergic and insulin deficiency should be considered.
Ketoacidosis in increased plasma K + is due
in the absence of insulin at pH absolute value. The 
blockers decrease the release of renin, which
values ​​fall aldosterone accentuate agonists
hyperkalemia.
6) Other considerations:
Hyperkalemic periodic paralysis: symptoms manifest
before any auspicious event hyperkalemia, being
this is the reason why the channels are open
sodium having the genetic mutation. Depending on
final voltage, the symptoms will go from one to myotonia
Total paralysis. The treatment is to avoid situations
leading to hyperkalemia (eg.: intense exercise);
empirically been shown symptomatic improvement with
acetazolamide (no known cause).
Chronic renal failure: elevation begins to observe
levels in plasma K + when GFR <20 ml="" p="">minute, which is more marked as it progresses
the renal function impairment.

TREATMENT

Treatment depends on the cause hyperkalemia

underlying and severity thereof.

Always try to determine the pathophysiological mechanisms involved in its genesis, to modify

and thus correct hyperkalemia. For example, in diabetic ketoacidosis, the pathophysiological mechanisms involved

in hyperkalemia are: insulin deficiency, hyperosmolarity due to hyperglycemia and metabolic acidosis, all

them responsible for the shift of K + from the extracellular space to

intracellular K + although the total body is often reduced by abundant secondary renal potassium excretion

to osmotic diuresis. The proper administration of insulin and electrolyte replacement reversed these disorders,

but it should be particularly careful with hypokalemia

that may occur as a result of treatment.

Whatever the cause, the treatment of hyperkalemia is based on three objectives:

Emergency treatment: antagonize toxic effect on the

heart (use of calcium).

Stimulate K + input to the intracellular space (use of

 2 agonists, insulin, glucose and bicarbonate).

Reduction of total body K + (diuretics resins,

cation exchange and dialysis).

Mild hyperkalemia (<6 .0="" div="" l="" meq="">

Elimination of the cause: stop taking diuretics

or K + sparing intravenous or oral intake, improve

acidosis or volume depletion, commencing replacement

hormone in cases of Addison (fludrocortisone initially

a dose of 100 g, initiating its action in 2 hours. And arriving at

Action peak a few days).

Use  2 agonists (Salbutamol) by nebulizer (consider sympathomimetic effects in cardiac patients).

With low urinary potassium can be tested with saline and loop diuretics to increase supply

distal sodium, generate higher volume and thus promote urinary excretion of potassium.

MODERATE hyperkalemia (6.0-7.0 mEq / L): a

It adds

Using polarizing solution (500 ml Dx 10% crystalline insulin 10 U) intravenously. The answer begins between

30 '- 60' (falling 1-2 mEq / L) and lasts several hours. It

can again be repeated if necessary.

Using sodium bicarbonate: is described the use of one ampoule

7.5% (44.6 mEq) to pass intravenously 5 ', the dose may be

Repeat every 10 ', especially in patients with acidosis. Without

But you should be very careful when you start

correct acidosis (patients may have seizures or tetany), can be generated volume surges

and should not be used in IRC.

Use of cation exchange resins (see below).

Severe hyperkalemia (> 7.0 mEq / L): Requires

aggressive treatment

Administration of calcium: Counter neuromuscular toxicity membranes, rapidly diminishing the risks of severe arrhythmias. The

dose is 10 ml of calcium gluconate 10% via

IV slowly (2'-5 'or less where digitalized patients). If no response to the 5 'can be applied

second dose. The effect lasts about 1 hour, with

which other therapies should be installed immediately.

NO Infuse CALCIUM BY THE SAME WAY THAT

BECAUSE BICARBONATE precipitate.

 Infusion of high doses of calcium can be toxic in digitalized patients

Using the methods described earlier: nebulized

 2 agonists, polarizing solution of glucose and insulin, Na bicarbonate.

Cation exchange resins:

They set the K + and exchange it for another cation (usually

1-2 mEq of Na + per 1 mEq of K +) in the gastrointestinal tract,

eliminating the body K +

Should be used as soon as possible, but with caution in patients who are intolerant of Na + overload

Initiate action in 1-2 hours, lasting 4-6 hours

They can be administered

to-mouth (of choice): astringent effect, administered with an osmotic agent (sorbitol). The starting dose is

15-30 mg of sodium polystyrenesulfonate mixed with 50

-100 Ml of 20% sorbitol. May be repeated up to 4-5 times

day. Adverse effect: nausea and vomiting.

b-rectally (when not tolerate oral or ileus exists): It

given 50 g of sodium mixed polystyrenesulfonate

with 200 ml of 20% glucose solution (never sorbitol)

being ideally retain the enema for 30'-60 '(rectal catheter

ball) and can be repeated up to 4 per day. later

must make cleansing enema to remove the resin.

- Hemodialysis effectively removes excess K + but

is reserved for patients where traditional methods fail or not be applied. Usually, then

of dialysis rebound hyperkalemia occurs by mobilization of intracellular stores.

chronic treatment

Patients with GFR <10 diet="" div="" follow="" min.="" ml="" should="">

restriction of K + (40 to 60 mEq / day)

They can be used loop diuretics

Exchange resins may be used 2 or 3 times a day,

at lower doses (5-10 g)

The oral bicarbonate can help in cases of acidosis

metabolic.