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Hyperkalemia & Hypokalemia

Hyperkalemia & Hypokalemia

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Hyperkalemia & Hypokalemia
Glen E. Hastings MDApril 27, 1999
I. Physiology:
 A.. Potassium’s 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. Theextracellular 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 for2 K
+
ions. This creates a negative (-75mV) charge across the resting membranes of the cells of thebody. Outward diffusion of K
+
ions through selective K
+
channels increases the negative electricalpotential further until at about –90mV the membrane depolarizes. This process drives nerve & muscleconduction, 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 & extracellularpH 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 cell’s basement membrane adjacent tothe 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 luminalsurface 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 dependentupon the availability of luminal Na
+
, low urinary K
+
concentrations & low urine osmolality. It is thereforerelated 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
+
conductancechannels (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. GIexcretion 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 corticalcollecting duct. In hypokalemia a TTKG <2 means that the cause is non-renal. In a hyperkalemicpatient, 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 hyperkalemialowers the depolarization threshold, part of the muscle tissue remains partially depolarized. Althoughthis 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 QRScomplex. Ventricular repolarization however, is enhanced, so the T waves become peaked. Withprogression these changes merge to form a “sign wave” pattern. Unfortunately, EKG changes are notsensitive indicators of the danger of asystole, or ventricular fibrillation, so treatment decisions should bebased 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 allcauses 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 inK
+
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, notinfrequently involving a prescription drug, coupled with age or disease related impairment of GFR, Renalexcretion of K
+
is decreased when GFR<25% of normal). A list if drugs most frequently implicatedalong 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 ActionDiet & Dietary SupplementPotassium SupplementsSalt Substitutes
Exogenous K
+
Exogenous K
+
 K Sparing DiureticsSpironolactoneAmilorideTriamterineAldosterone AntagonismNa
+
channel blockade in principal cellsNa
+
channel blockade in principal cellsAngiotensin II BlockersACE InhibitorsAT II Receptor Blockers
Aldosterone, RBF & GFR.
Aldosterone, RBF & GFR.Antiinflammatories NSAIDS
Renin, Aldosterone, RBF & GFR.Adrenergic Drugs
β
-Blocking Agents
α
-Adrenergic AgonistsImpaired Cellular Glucose UptakeImpaired Cellular Glucose UptakeAntibioticsTrimethoprimPotassium Penicillin GPentamidineNa
+
channel blockade in principal cells
Exogenous K
+
Na
+
channel blockade in principal cellsImmune Modulating DrugsCyclosporineTacrolimus
Aldosterone Release, &
Na
+
 / K
+
ATPase Activity
Aldosterone Release, &
Na
+
 / K
+
ATPase ActivityMiscellaneousSuccinylcholineDigoxinHeparinK
+
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, astate of “ineffective circulating blood volume” occurs where insufficient Na is delivered to the corticalcollecting 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 withhypoaldosteronism or aldosterone resistance. It is common in acute renal failure caused by acutetubular necrosis because of concomitant metabolic acidosis & K
+
release secondary to hemolysis ortissue necrosis. Acute glomerulonephritis, sickle cell disease, interstitial nephritis, systemic lupuserythematosus, 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 hyporeninemichypoaldosteronism, a condition usually occurring in diabetic patients or those with chronic interstitialnephritis & 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 mayprecipitate life threatening hyperkalemia. The condition is treated with low K
+
diet & loop or thiazidediuretics combined with NaHCO
3
. 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 Addison’s disease 
. The most common form of congenital adrenal hyperplasia is
21-hydroxylase deficiency 
whichimpairs 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 acquiredform occurs as a result of tubulointerstitial dysfunction in such conditions as amyloidosis, chronicpyelonephritis, or obstructive uropathy. Both feature salt wasting, hypovolemia, & hyperkalemia butdiffer 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 hyperchloremicacidosis with hyperkalemia. The most common intermediate causes are insufficient aldosteroneproduction 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:
Gordon’s syndrome features hyperkalemia, & volume expansion with related hypertension, in patientswith normal renal function. It results from a selective increase in the tubular reabsorption of Cl whichexpands circulating volume depressing renin & aldosterone. Treatment with thiazides. Selectivedefects 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, transfusionreactions or stored blood administration may produce hyperkalemia. Vigorous physical exercise alonemay 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 theiraccompanying anions are distributed to both the intracellular & extracellular compartments & do nottherefore cause a K shift. Metabolic acidosis caused by inorganic acids and conditions like diabeticketoacidosis featuring hypertonicity are frequent causes of hyperkalemia, best treated by remedying theprecipitating 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 bydysfunction of the sodium channels of the muscles of the limbs resulting in periodic episodes ofweakness 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 isessential.
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
:

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