R4 Hypokalemia and hyperkalemia

  1. Hypokalemia and hyperkalemia
    Hypokalemia - serum potassium concentration less than the normal range of 3.5-5.5mEq/L

    Hyperkalemia - serum potassium concentration greater than the normal range of 3.5-5.5mEq/L
  2. Potassium balance
    • ICF (98%) >>>>>> ECF
    • Intra-cellular vs extra-cellular balance; intracellular balance is critical for minimizing transient changes in serum K+
    • Urine is major excretory pathway; stool in some  states

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  3. Regulation of internal balance of K+
    1. β2 agonists - catecholamines for tx of asthma, hypertension, angina

    • 2. insulin - diabetes mellitus
    • - often used in the treatment of high K+ (shifts K+ into cells)

    3. Body fluid tonicity - diabetes mellitus

    4. hypertonicity effects water and K+ movement out of cells (solvent drag)

    • 5. acid-base balance -- intracellular buffering (K-H exchange)
    • -Mineral acidosis, metabolic alkalosis

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  4. Regulation of external potassium balance
    • Intake: rarely the problem
    • -High intake rarely causes high serum K, unless there are reasons for compromised excretion or internal balance
    • -low intake rarely causes low serum K, unless it is coupled to augmented excretion

    • Excretion:
    • -Kidney>>>>>GI tract (90%/10%)
    • -Urine K+ varies with intake; kidney can increase K+ excretion rapidly in response to increase in serum K
    • -Kidney conservation of K is less rapid (days to weeks to maximize)
  5. K+ in the nephron
    • filtered at glomerulus
    • reabsorbed by proximal tubule and TAL
    • excretion (and serum concentration**) controlled by distal tubular secretion (DCT)
    • -excretion is highly regulated

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    • Regulation of distal tubular K+ secretion: increases/decreases
    • 1. Serum K+
    • 2. Aldosterone/responsiveness to aldosterone
    • 3. Distal tubular flow rate 
    • -increased flow leads to kaliuresis (volume expansion, 1o hyperaldosteronism, diuretics acting proximal to DCT, osmotic diuretics, metabolic alkalosis)
    • -decreased flow can lead to K+ retention (volume depletion, low effective arterial volume; K-losing tendencies of primary hyperaldosteronism is blunted by low sodium intake)

    • 4. Acid-base balance
    • -alkalemia increases (and acidemia decreases) uptake of potassium from peritubular capillary into the tubular epithelial cell
    • -Acute metabolic/respiratory alkalosis enhances K+ secretion and excretion
    • -Acute metabolic/respiratory acidosis blunts potassium secretion/excretion
    • -Chronic metabolic alkalosis shows marked kaliuresis, low serum potassium, very low total body potassium

    • -Acidosis: decreased potassium secretion/excretion
    • -Alkalosis: increased potassium secretion/excretion

    5. Drugs (K-sparing diuretics)

    6. Anion delivery

    7. Sodium delivery
  6. Clinical approach to K+ imbalances
    • -History, physical
    • -medication use
    • -lab vallues
    • -TTKG

    *Most patients with hyperkalemia have multiple defects in potassium homeostasis

    • Transtubular K+ Gradient:
    • -used to assess whether the kidneys are responding appropriately to the low or high K+
    • -reflects the driving force for K+ secretion in CD
    • -TTKG = [UK+/blood K+] x Posm/Uosm

    • Nl kidney: problem is extra-renal
    • -Hyperkalemia: TTKG >6
    • -Hypokalemia: TTKG <3

    • Abnormal kidney: problem with the kidney
    • -hyperkalemia: TTKG <6
    • -hypokalemia: TTKG >3

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  7. Hyperkalemia with increased TTKG
    Hyperkalemia is due to extra-renal problem

    • 1. Increased intake
    • -Fruits, Vegetables

    • 2. Cellular shift
    • -Pseudohyperkalemia
    • -Acidosis
    • -Insulin deficiency
    • -β-blockers
    • -Digoxin
    • -Tissue necrosis
    • -Periodic paralysis
  8. Hyperkalemia with low TTKG
    TTKG <6
    Hyperkalemia related to impaired renal function

    • 1. Hypoaldosteronism
    • -Spironalactone
    • -NSAIDs
    • -ACE-In
    • -ARB
    • -Renin inhibitor
    • -Type 1 and 2 PHA
    • -Adrenal insufficiency
    • -Hyporeninemia

    • 2. Reduced Na+ uptake
    • -Decreased ECV
    • -Triamterene
    • -Amiloride

    • 3. Low GFR
    • -Acute and chronic kidney disease
  9. Consequences of hyperkalemia
    • Abnormal cardiac muscle depolarization and repolarization
    • -Peaked T waves
    • -Shortened QT interval
    • -Widening of QRS
    • -disappearance of the P wave
    • -"sine wave pattern"
    • -Ventricular fibrillation
    • -skeletal muscle weakness (completely unimportant finding)

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  10. Treatment of hyperkalemia
    • Rule out pseudohyperkalemia
    • -lab error due to lysis of cells in tube; leukocytosis and thrombocytosis
    • -repeat with fresh blood draw

    *Tx not evidence based in terms of what Rx to give at what K+ level

    • Tx that promotes K+ shift into cells
    • 1. Calcium chloride
    • -K+ raises the resting membrane potential; Ca2+ raises the threshold potential so that the difference is what it normally is (or near normal)
    • -temporary effect: lasts ~1hr

    • 2. IV insulin and glucose
    • -drives K+ into the cells
    • -lasts for hrs

    • 3. Nebulized salbutamol (β agonist)
    • -lasts for hrs

    • Tx that promotes K+ loss
    • 1. Cation exchange resin (Kayexelate)
    • -causes diarrhea

    2. Loop diuretics (if normal ECV)

    3. Dialysis (if ESRD)
  11. Hypokalemia
    • Inadequate intake (rare)
    • Cellular uptake
    • Nonrenal loss
    • Renal loss (high blood pressure vs normal/low BP)
  12. Hypokalemia with low TTKG
    Extrarenal cause for hypokalemia - kidney is trying to hold on to K+

    • 1. Decreased intake
    • -Geophagia ('eating dirt')

    • 2. Cellular shift
    • -Alkalosis
    • -Insuline/Glucose
    • -β2-agonists
    • -Cell proliferation
    • -Periodic paralysis

    • 3. GI loss
    • -Diarrhea
    • -Laxative abuse
  13. Hypokalemia with increased TTKG
    TTKG >3
    Hypokalemia due to renal problem; inappropriately elevated TTKG

    • Evaluation:
    • 1. BP
    • 2. pH (if blood pressure is normal or low)
    •      A. RTA (if pH is low)
    •      B. Vomiting, Diuretics, Bartter's syndrome, Gitelman's syndrome (if pH is high)
    • 3. Renin (fi blood pressure is high)
    •      A. Renal arterial stenosis (if Renin is high)
    • 4. Aldosterone (if renin is low)
    •      A. Primary hyperaldosteronism, GRA (if Aldosterone is high)
    •      B. Cushing's syndrome, congenital adrenal hyperplasia, AME, LIddle's syndrome (if Aldosterone is low)
  14. Treatment of hypokalemia
    • -Estimate K+ deficit; but complicated due to alterations in internal balance
    • -If uncomplicated, plasma K decreases by approximately 0.3mEq/L for each decriment of 100mEq total body K

    • -Asymptomatic: hypokalemia is treated with oral KCl replacement
    • -IV KCl can be used in pts with symptoms

    • -Rate of replacement: must consider severity of the hypokalemia, pt's underlying disease
    • -Avoid rates >10-20mEq/hr (risk of overcorrecting to hyperkalemia)
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R4 Hypokalemia and hyperkalemia
hypokalemia and hyperkalemia