Lecture 2: Electrolyte Disorders I

Mild Hyponatremia

Na

Arginine Vasopressin (AVP)

-Also called vasopressin or antidiuretic hormone (ADH).

-A peptide hormone from the posterior pituitary that promotes water conservation.

Dehydration

high sodium and low volume = __________________

Overhydration

low sodium and high volume = ___________________

135-145 mEq/L

normal sodium levels

Severe Hyponatremia

Na

50

if [Na] is

Hyponatremia

-Mild: nausea and malaise

-Moderate: headache, nausea, disorientation confusion, agitation, ataxia, areflexia

-Severe: intractable vomiting, seizures, coma, ultimately respiratory arrest due to brainstem herniation

Step 1: Determine plasma osmolality

Step 2: In hypotonic, determine urine osmolality

Step 3: If urine Osm >100, determine volume status and urine sodium

What are the steps of hyponatremia evaluation?

Osmolar Gap

measured osmolality - calculated osmolality

True Hyponatremia

-low Osmolality (

False Hyponatremia

-normal osmolality (285-295 mmol/L)

-lab error

-hyperlipidemia

-hyperproteinemia

-multiple myeloma

False Hyponatremia

-high osmolality (>295 mmol/L)

-serum increased concentration of effective osmoles

-mannitol, glucose, glycine

1.6

Each 100 mg/dL increase in plasma glucose above 100 mg/dL decreases serum sodium by ________ mEq/L

Diluted

Sodium is ____________ when water intake exceeds water output

Dependent

ADH ______________________ Hypo-osmolar Hyponatremia:

-High (>200-300 mOsm/kg)

-Check volume status

-Hypervolemic - heart failure

-Hypovolemic - Loss of fluid

-Euvolemic - hormone related

Independent

ADH _____________________________ Hypo-osmolar Hyponatremia:

-Low (

Hypovolemic

-dehydrated

-Urine Na < 20; high Uric H+

-Renal Losses (U-Na>20)

-GI Losses

-Other: Skin, lungs, etc

Euvolemic

-Urine Na > 20; low Uric H+

-Hypothyroid

-Adrenal Insufficiency

-SIADH

-Cerebral Salt Wasting

Hypervolemic

-edema

-Urine Na < 20; High Uric H+

-Heart Failure

-Liver Failure

-Nephrotic syndrome

Diuretics

Urine sodium not accurate in patients on ________________

SIADH

• Diagnosis of exclusion, check thyroid panel, cortisol levels

• ADH lowers water excretion (causes naturesis), intake easily exceeds output

• Uric acid is suppressed and may drop below normal.

• Often transient. If persistent, look for causes: CNS, malignancy, drugs

-Fluid restriction

-Low dose loop diuretic

-Solute load (salt tabs or ure-na)

Treatment for SIADH

-SSRIs

-Anti-epileptics

-Sulfonylureas

-Opiates

meds that cause SIADH

Acute Hyponatremia

-

Chronic Hyponatremia

->48 hours

-defect in excretion/reabsorption of sodium

• Lower rate of excretion due to low volume of distal delivery of filtrate

• Vasopressin actions, lowering rate of water excretion (SIADH)

• Rapidly increase sodium by 4-6 mEq/L

• Infuse with 3% hypertonic saline (100 mL bolus over 10 minutes, repeat up to 3 times, until symptoms improve)

Treatment of acute hyponatremia with severe symptoms (coma, seizures, etc)

• Aim to increase sodium by 5 mEq/L daily, not exceeding 6 mEq/L

• Change in Plasma Na = (infusion[Na]-serum[Na])/(TBW+1)

Treatment of mild-moderate symptoms or chronic hyponatremia

• D/C ongoing active treatment

• Start D5W

• Add DDAVP

treatment for hyponatremia IF overcorrected (>10 mEq/L in first 24 hrs)

Vaptans

-AVP antagonists

-cause you to excrete dilute urine

-unpredictable increases in serum sodium

-expensive

-risk of liver toxicity

Shrink

too rapid correction of hyponatremia cause cause cells to _______________

Hypernatremia

• Usually results from a deficit of TBW or net gain of Na.

• Symptoms more evident with rapid changes, due to cell shrinking

• Nausea, vomiting, lethargy, weakness, polyuria

Hypernatremia

• Generally, a patient with an impaired sense of thirst, or limited access to water.

• Risk factors: elderly, infants, decompensated diabetes, hospitalized patients.

Cerebral Edema

rapid correction of hypernatremia can result in ___________________

Hypernatremia

Risk factors:

• >65 years old

• Mental or physical disability with impaired thirst

Hypernatremia

Causes:

• Diuretics

• Osmotic diuresis

• Renal salt wasting

• Post obstructive diuresis

• Diuretic phase of ATN

• GI (diarrhea/vomiting) and cutaneous (excessive sweating/heat/exercise)

Large sodium ingestion (like sea water)

if someone has hypernatremia and is hypervolemic, assess for _________________________________

Extrarenal Losses (GI, sweat, vent)

if someone has hypernatremia and is hypovolemic and:

-If urine osmolality >800 and FeNa

Diabetes Insipidus

if someone has hypernatremia and is hypovolemic and:

If urine osm 300-800, this suggests ________________________

Diabetes Insipidus

condition where kidney is unable to resorb free water

Central

____________________ Diabetes Insipidus:

-inadequate ADH production

Nephrogenic

____________________ Diabetes Insipidus:

-ineffective ADH receptors

Treat Underlying Cause

treatment for Nephrogenic Diabetes Insipidus

Trial DDAVP- PN 10 mcg/q12hr

treatment of Central Diabetes Insipidus

• If there is a response - central DI

• If no response, nephrogenic DI

What do you do for Diabetes Insipidus after DDAVP trial?

D5W (Dextrose in Water or basically just pure water with some sugar) at a SLOW

treatment for hypernatremia greater than 48 hours or not sure

-D5W (Dextrose in Water or basically just pure water with some sugar)

-Can be given at a quicker rate

treatment for hypernatremia less than 48 hours

10-12

treatment goal for hypernatremia is _________ mmol/day correction

K+

-the major intracellular cation

-used to balance intracellular anions

Muscle

majority of body potassium is where?

0.1; 0.6

For over __________ decrease in pH, [K+] rises by __________ mEq/L

Hypokalemia

• Cell membrane partially depolarized, diminished sodium permeability, decreased action potentials

Hypokalemia

-ECG: ST depressions, t-wave flattening, U wave, QT prolongation

• Sinus tachycardia, torsades de pointes, atrial fibrillation,

ventricular rhythms (VT/VF/ectopy)

Hypokalemia

• Fatigue, weakness, palpitations, paralysis (periodic paralysis)

• Paralytic ileus, myopathy, rhabdomyolysis - 2/2 muscle ischemia

Hypokalemia

1. Insufficient dietary intake (fasting, eating disorder, alcoholism)

2. Intracellular shifts

3. Increased losses

most frequent causes of hypokalemia

Glucose/Insulin

rapidly shifts potassium into cells

Alkalosis

-condition that causes potassium to follow hydrogen ions

-intracellular shift

Beta 2-Agonists (Asthma)

drugs that cause an intracellular shift of potassium

Hypokalemia

Causes:

• Renal tubular acidosis - causes alkalotic state and shift

• Hyperaldosteronism

• Magnesium Depletion

• Leukemia

• Vomiting

• Diarrhea

• Laxatives

• Ileal loop

2.5 mEq/L

Hypokalemia symptoms start when K+ levels are < _________

• Loop diuretics

• Thiazide diuretics

• Magnesium deficiency

• Bartter/Gitelman syndrome

what can cause urine chloride to be high?

-Adrenal adenomal

-Glycocorticoid suppressible hyperaldostronism

What can cause low renin, high aldosterone and >13 mEq/g Creatinine?

• Renal Artery Stenosis

• Renin secreting tumor

What can cause high renin and high aldosterone and >13 mEq/g Creatinine?

• Cushings

• Liddle Syndrome

What can cause low renin and low aldosterone and >13 mEq/g Creatinine?

Bartter's Syndrome

-cause of hypokalemia

-mutations in sodium-potassium-chloride co-transporter at the TAL of loop of henle

• 5 subtypes

• Associated with metabolic alkalosis, hypercalciuria, salt wasting, kidney stones.

• *Normal blood pressure.

Bartter's Syndrome

What conditions presents as a loop diuretic?

Gitelman's Syndrome

-cause of hypokalemia

- gene mutation causing salt wasting, and secondary hyperaldosteronism, decreased absorption of sodium in the distal tubules

• Hypocalciuric

• Hypomagnesemia

• Hypokalemic Periodic Paralysis

Fanconi's Syndrome

-failure to reabsorb bicarb which leads to metabolic acidosis, excretion of K and Ca

-nephrogenic DI

- replace orally

• Can give 100-150 mEq/day safely

• Liquid is bitter, both irritating

• Generally 10 mEq for every 0.1 mEq/L

treatment for mild hypokalmeia (>3)

- IV replacement

• Give 100 mEq for every 0.3 mEq/L deficit

• Peripheral - 10 mEq/hr

• Central - 20 mEq/hr

treatment for severe hypokalemia (

Glucose solutions

what should you avoid in hypokalemia treatments?

Magnesium (20-60 mEq/24hr)

In treatment of hypokalemia, you should also replace __________________ because it optimizes tubular uptake of K+

Hyperkalemia

• Commonly a lab error due hemolysis during phlebotomy

• Clinical manifestations due to disordered membrane polarization:

• Resting potential of myocardium, slower/reduce amplitude of action potential

Hyperkalemia

Symptoms: neuromuscular dysfunctional weakness, paresthesias, areflexia, ascending paralysis, GI effects (N/V/D)

Hyperkalemia

-prolonged PR, tall peaked T waves, short QT

-Flattened P wave

-Widening QRS

-QRS degradation into sinusoidal pattern

Extrarenal

Spot urine K > 20 mEq/L means it is a ______________ cause

oliguric kidney failure, or ACE/ARB effect

Urine K

Hyperkalemia

Causes:

• Excessive intake (melons, citrus juice)

• Cellular redistribution - tissue damage, tumor lysis

• Decreased renal excretion

• Decreased distal delivery of sodium

• Decreased mineralocorticoid activity

• Distal tubular defect

Hyperkalemia

• Calcium chloride 5-10 mL IV

• Calcium gluconate 10-20 mL IV

Hyperkalemia treatment: membrane stabilization

a) NaHCO3 - 50-150 mEq IV if met acidosis present

b) Albuterol - 10-20 mg/4mL over 10 minutes

c) Insulin/glucose - 5-10 Units IV/25g glucose (sometimes start d10W drip)

Hyperkalemia treatment: shifting potassium into cells

Furosemide 40-80 mg IV

Hyperkalemia treatment: renal excretion

a) Sodium zirconium cyclosilicate

b) Sodium polystyrene sulfonate

Hyperkalemia treatment: binds K+ in GI tract

Hemodialysis

Hyperkalemia treatment:

Removes K+