L3 - Fluid and Electrolyte Disorders pt 2

Define hyperkalemia

Potassium > 5.5 mEq/L

What are some causes of hyperkalemia?

Increased intake

Decreased renal elimination (renal failure, tumor lysis syndrome)

Decreased response to aldosterone

Redistribution of K+ from ICF to ECF (hemolyzed sample)

Give the symptoms of severe (>7 mEq/L) hyperkalemia

Heart palpitation, ECG changes (Peaked T waves, wide QRS), arrhythmias, etc.

1. What is the first step in treating someone with hyperkalemia?

Determine if they have an abnormal ECG

1. Describe the treatment recommended if a hyperkalemic patient has an abnormal ECG

Administer calcium gluconate (peripherally IV) or calcium chloride (central IV)

What does IV calcium do in hyperkalemia?

It stabilizes the cardiac cell membrane by raising the threshold potential, making cardiac cells less likely to depolarize inappropriately. It reduces the risk of arrhythmias but does not lower serum potassium.

2. Describe the treatment recommended if a hyperkalemic patient has a normal ECG

AND

Describe the treatment recommendation for a hyperkalemic patient with abnormal ECGs after calcium administration

Determine if the patient is hyperglycemic (>250 mg/dL)

2. Describe the treatment recommended if a hyperkalemic patient is hyperglycemic (> 250mg/dL)

Give insulin WITHOUT dextrose and follow blood sugar

Why is insulin given without dextrose in hyperkalemic patients who have hyperglycemia?

Insulin drives K⁺ into cells via the Na⁺/K⁺ ATPase. It's usually paired with dextrose to prevent hypoglycemia, but in hyperglycemia, extra dextrose isn't needed and would worsen high blood sugar.

2. Describe the treatment recommended if a hyperkalemic patient is not hyperglycemic (< 250mg/dL)

Give insulin WITH dextrose

Why is insulin with dextrose given in a hyperkalemic patient who is not hyperglycemic (

Insulin shifts K⁺ into cells via the Na⁺/K⁺ ATPase. If glucose is

3. Describe the treatment recommendation for a hyperkalemic patient after insulin administration

Consider albuterol

Why is albuterol recommended in hyperkalemic patients?

Albuterol (β₂ agonist) activates the Na⁺/K⁺ ATPase, shifting potassium from the blood into cells. This lowers serum K⁺ quickly, especially as an add-on to insulin therapy.

4. Describe the treatment recommendation for a hyperkalemic patient after albuterol administration

Consider sodium bicarbonate if acidic (pH < 7.2)

Why is sodium bicarbonate recommended in hyperkalemic patients?

It raises blood pH, which drives H⁺ out of cells and K⁺ into cells (via H⁺/K⁺ exchange). It is especially useful if the patient also has metabolic acidosis.

5. Describe the treatment recommendation for a hyperkalemic patient after sodium bicarbonate administration

Consider dialysis or exchange resin

Why consider dialysis or exchange resins in hyperkalemia?

Unlike calcium, insulin, albuterol, or bicarbonate (which only shift K⁺ into cells temporarily), dialysis and potassium exchange resins actually remove K⁺ from the body, making them definitive treatments.

What are exchange resins?

Medications that bind potassium in the gut and exchange it for another ion (like sodium or calcium), so K⁺ is eliminated in the stool.

What are alternative therapies for hyperkalemia?

Kayexalate (for chronic management only).

Loop diuretics (if normal renal function).

Hemodialysis (if renal failure).

Define hypomagnesemia

Magnesium < 1.4 mEq/L

Name three hypomagnesemia etiologies

GI loss, renal loss, and medication-induced loss

Name a drug that induces GI loss of magnesium

Laxatives such as magnesium citrate

(Theoretically, someone could get hypermagnesemia if they take too much, but it acts more as a laxative)

Name diuretics that induce loss of magnesium

Furosemide, torsemide, bumetanide, HCTZ, and chlorothiazide

Name an antifungal drug that induces loss of magnesium

Amphotericin B

(also causes DI and hypokalemia)

Name two anti-rejection drugs that induce loss of magnesium

Tacrolimus and cyclosporine

Is hypomagnesemia usually symptomatic or asymptomatic?

Asymptomatic.

What electrolyte abnormalities can result from hypomagnesemia?

Low calcium (hypocalcemia) and low potassium (hypokalemia).

What neuromuscular symptoms can occur in hypomagnesemia?

Twitching, tetany, and seizures.

What cardiovascular symptoms can occur in hypomagnesemia?

Palpitations and ECG arrhythmias (e.g., wide QRS, peaked T waves).

What treatment is recommended for those with mid-moderate hypomagnesemia?

Supplement with magnesium oxide or antacids

What treatment is recommended for those with severe hypomagnesemia?

Magnesium sulfate via IV

Can add magnesium sulfate to maintenance fluids as well

Define hypermagnesemia

Magnesium > 2 mEq/L

What are two causes of hypermagnesemia?

Decreased renal excretion or increased intake

What neuromuscular symptoms occur in hypermagnesemia?

Hypotonia, paralysis, and coma.

What respiratory symptoms occur in hypermagnesemia?

Respiratory depression.

What cardiovascular symptoms occur in hypermagnesemia?

Hypotension, arrhythmias, and ECG changes (QT and PR prolongation)

Describe the first-line treatment recommended for a hypermagnesemia patient who has an abnormal ECG

Administer calcium gluconate (peripherally IV) or calcium chloride (central IV)

What does IV calcium do in hypermagnesemia?

It stabilizes the cardiac cell membrane, making the heart muscle cells less likely to depolarize inappropriately. It reduces the risk of arrhythmias, but it does not lower magnesium.

Describe the second-line treatment recommended for a hypermagnesemia patient

Increase renal elimination of magnesium

Normal kidney: isotonic fluid bolus or loop diuretics

Kidney failure: dialysis

Note: Why is a fluid bolus given to a patient with hypermagnesemia?

A fluid bolus is given in hypermagnesemia to enhance renal clearance of magnesium by increasing GFR and urine output

Describe the third-line treatment recommended for a hypermagnesemia patient

Decrease magnesium intake

What triggers PTH release? How does PTH affect bone?

Low blood calcium stimulates the parathyroid glands to release PTH.

PTH stimulates osteoclast activity → bone resorption → releases both calcium and phosphate into the blood.

How does PTH affect the kidneys in terms of calcium and phosphate?

PTH makes kidneys reabsorb calcium (keep it) and excrete phosphate (lose it).

What is the net effect of PTH on blood calcium and phosphate?

Increases calcium and decreases phosphate, preventing calcium-phosphate precipitation in tissues.

Describe how calcium and phosphorus concentrations are related

Calcium and phosphate are inversely related due to PTH.

Low Ca²⁺ → PTH ↑ → Ca²⁺ rises, phosphate excreted (↓ PO₄³⁻).

High Ca²⁺ → PTH ↓ → Ca²⁺ falls, phosphate retained (↑ PO₄³⁻).

What triggers calcitonin release? How does calcitonin affect bone?

High blood calcium levels stimulate calcitonin secretion from the thyroid C-cells. It inhibits osteoclast activity, which decreases bone resorption and lowers blood calcium levels.

Describe calcium found in the ECF

Half of the calcium in the ECF is attached to proteins such as albumin. However, the unbound calcium is the active form

Why can total calcium appear falsely low when albumin is low?

Because ~50% of calcium is bound to albumin. When albumin decreases, bound calcium decreases, but ionized (active) calcium stays normal. Body function isn't altered

What is the equation for corrected calcium?

[measured Ca2+] + [(4-albumin) x 0.8]

Describe phosphorus

Part of nucleic acids and ATP, needed for normal bone and tooth structure

How does renal function influence phosphorus levels?

Kidneys regulate phosphate by excreting or reabsorbing it.

Define hypocalcemia

Calcium < 8.5 mg/dL

Name some hypocalcemia etiologies

Hypoparathyroidism (less PTH, less calcium conc), vitamin D deficiency, severe hypomagnesemia, and medication-induced

What are some medications that induce hypocalcemia?

- Loop diuretics such as furosemide, bumetanide, and torsemide

- Calcitonin

What neurologic symptoms occur in hypocalcemia?

Tetany, muscle cramps, and seizures.

What cardiovascular symptoms occur in hypocalcemia?

Hypotension, arrhythmias, and ECG changes (e.g., prolonged QT interval).

Name some treatments of asymptomatic hypocalcemia

Oral calcium supplements and vitamin D supplements

Name some treatments of symptomatic hypocalcemia

Initial bolus dose: calcium gluconate (peripheral) or calcium chloride (central)

Maintenance dose: add calcium to IV fluids

Define hypercalcemia

Calcium > 10.5 mg/dL

What are some etiologies of hypercalcemia?

Cancer, hyperparathyroidism, granulomatous disease, and medication-induced

Name some medications that induce hypercalcemia

Thiazide diuretics (decrease calcium excretion), vitamin D, calcium supplements, and aluminum/magnesium antacids (chelation)

What are some symptoms of hypercalcemia levels

Asymptomatic

What are the renal manifestations of hypercalcemia (> 12 mg/dL)?

Nephrolithiasis, and acute and chronic renal failure

What are the cardiovascular manifestations of hypercalcemia (> 12 mg/dL)?

ECG changes: shortened QT interval

Hypertension

Arrhythmias (e.g., tachycardia)

What are the neurological manifestations of hypercalcemia (> 12 mg/dL)?

Alerted mental status, coma, etc.

What are the GI manifestations of hypercalcemia (> 12 mg/dL)?

Severe constipation, N/V, etc.

What are the treatments recommended for a patient with symptomatic hypercalcemia with normal kidney function?

1. Isotonic fluid bolus (aids in volume depletion and excreting calcium)

2. Loop diuretic

3. Calcitonin

4. Glucocorticoid (reduces intestinal calcium absorption and decreases bone resorption)

What are the treatments recommended for a patient with symptomatic hypercalcemia with kidney failure?

1. Hemodialysis

2. Calcitonin

3. Glucocorticoid

What are the treatments recommended for a patient with asymptomatic hypercalcemia < 12 mg/dL?

Monitor, eliminate, and treat the underlying cause

What are the treatments recommended for a patient with asymptomatic hypercalcemia > 12 mg/dL?

1. Isotonic fluid bolus

2. Loop diuretic

3. Caclitonin

4. Glucocorticoid

5. IV bisphosphonate (works slowly, more chronic treatment, such as cancer. Phosphate and calcium are inversely related!)

Define hypophosphatemia

Phosphorus < 2 mg/dL

What drugs decrease GI absorption, leading to hypophosphatemia?

Phosphate binders such as sucralfate, sevelamer, and calcium carbonate.

What drugs increase urinary excretion, leading to hypophosphatemia?

Acetazolamide

What drugs cause intracellular or intestinal redistribution, leading to hypophosphatemia?

Insulin therapy: shifts phosphorus into cells

Diabetic ketoacidosis: insulin for treatment shifts phosphorus into cells

Alcoholism

What neurologic symptoms occur in hypophosphatemia?

Metabolic encephalopathy (confusion, delirium).

What cardiovascular symptoms occur in hypophosphatemia?

Decreased contractility, heart failure, and respiratory failure.

What musculoskeletal symptoms occur in hypophosphatemia?

Myopathy (muscle weakness).

What is the main reason for all symptoms of hypophosphotemia?

Low phosphorus means low ATP. ATP is needed for many functions, including muscle contraction and brain energy

How is asymptomatic hypophosphatemia (or serum phosphorus 1-2 mg/dL) treated?

Oral phosphate salts (sodium or potassium).

Note: Osmotic diarrhea is a common side effect.

How is symptomatic hypophosphatemia (or serum phosphorus

Initial bolus: IV sodium phosphate or potassium phosphate over 4-6 hours.

Maintenance: Add sodium or potassium phosphate to IV fluids.

Define hyperphosphatemia

Phosphorus > 4.5 mg/dL

What are common causes of hyperphosphatemia due to decreased GFR?

Chronic kidney disease or acute kidney injury means phosphate is not excreted effectively by the kidneys.

What iatrogenic causes can lead to hyperphosphatemia?

Sodium phosphate-containing enemas (e.g., Fleet's enema)

Bisphosphonates: etidronate, pamidronate, zoledronate

What other conditions can cause hyperphosphatemia?

Rhabdomyolysis (rapid breakdown of muscle releases phosphate into the blood).