Chapter 9: Fluids and Electrolytes Flashcards by P H

Water distribution

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Determines intracellular/extracellular osmotic pressure

Sodium

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MCC is iatrogenic; first sign is weight gain

Volume overload

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What is the first sign of volume overload?

Weight gain

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Can release a significant amount of water

Cellular catabolism

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Normal saline: [Na], [Cl]

[Na] = 154 [Cl] = 154

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3% Normal saline [Na], [Cl]

[Na] = 513 [Cl] = 513

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Lactated ringer’s [Na], [K], [Ca], [Cl], [Bicarb]

[Na] = 130 [K] = 4 [Ca] = 2.7 [Cl] = 109 [Bicarb] = 28

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Calculate plasma osmolarity

(2Na) + (Glucose/18) + (BUN/2.8)

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Normal plasma osmolarity

280 - 295

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How does water achieve osmotic equilibrium?

Water shifts from areas of low solute concentration (low osmolarity) to areas of high solute concentration (high osmolarity) to achieve osmotic equilibrium.

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Estimates of volume replacement

4 cc/kg/h for 1st 10kg 2cc/kg/h for 2nd 10kg 1 cc/kg/h for each kg after that

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Best indicator of adequate volume replacement

Urine output

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Fluid loss during abdominal operations

0.5 - 1.0 L/h unless there are measurable blood losses

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When should you think about replacing blood?

> 500 cc

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What are insensible fluid losses?

10 cc/kg/day; 75% skin, 25% respiratory, pure water

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Replacement fluids after major adult gastrointestinal surgery: 1st 24 hours -> After 24 hours ->

1st 24 hours: LR After 24 hours: D5 1/2 NS with 20 mEq K+

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Why switch to D5 1/2 after 24 hours with replacement fluids after major adult gastrointestinal surgery?

5% dextrose will stimulate insulin release, resulting in amino acid uptake and protein synthesis (also prevents protein catabolism)

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How much glucose does D5 1/2 NS @ 125/h provide?

150g glucose per day (525 kcal/day)

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GI fluid secretion: Stomach

1-2 L/day

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GI fluid secretion: Biliary system

500 - 1,000 mL/day

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GI fluid secretion: Pancreas

500 - 1,000 mL/day

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GI fluid secretion: Duodenum

500 - 1,000 mL/day

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Normal K+ requirement

0.5 - 1.0 mEq/kg/day

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Normal Na+ requirement

1 - 2 mEq/kg/day

Electrolyte loss: sweat

Hypotonic (Na concentration 35-65)

Electrolyte loss: saliva

K+ (highest concentration of K+ in body)

Electrolyte loss: stomach

H+ and Cl-

Electrolyte loss: pancreas

HCO3-

Electrolyte loss: bile

HCO3-

Electrolyte loss: small intestine

HCO3- and K+

Electrolyte loss: large intestine

K+

Replacement: gastric losses

Replacement is D5 1/2 NS with 20 mg K+

Replacement: pancreatic / biliary / small intestine losses

Replacement is LR with HCO3-

Replacement: large intestine losses (diarrhea)

Replacement is LR with K+

Replacement: GI losses

Should generally be replaced cc/cc

Replacement: Dehydration (eg marathon runner)

Replacement with normal saline

Replacement: urine output

Should be kept at least 0.5 cc/kg/h; should not be replaced, usually a sign of normal postoperative diuresis

Peaked T waves on EKG; often occurs with renal failure Tx?

Hyperkalemia - Calcium gluconate (membrane stabilizer for heart) - Sodium bicarbonate (causes alkalosis, K enters cell in exchange for H) - 10U insulin, 1 amp D50 (K driven into cells with glucose) - Kayexalate - Dialysis if refractory

T waves disappear (usually occurs in setting of overdiuresis)

Hypokalemia - May need to replace magnesium before you can correct K+

First-line treatment for hyponatremia

Water restriction, then diuresis

Why correct sodium slowly?

Avoid central pontine myelinosis (no more than 1 mEq/h)

How does sugar affect sodium?

Hyperglycemia can cause pseudohyponatremia - for each 100 increment of glucose over normal, add 2 points to the sodium value

How does SIADH affect sodium?

SIADH: syndrome of inappropriate antidiuretic hormone can cause hyponatremia

MC malignant cause of hypercalcemia

Breast cancer

MC benign cause of hypercalcemia

Hyperparathyroidism

Tx: hypercalcemia - General disease - Malignant disease

- General: NS at 200-300 cc/h and Lasix - Malignant: mithramycin, calcitonin, alendrotnic acid, dialysis

Why no LR or thiazide diuretics in hypercalcemia?

LR: contains calcium Thiazide diuretics: retain calcium

Hypocalcemia: S&S

Hyperreflexia, Chovstek's sign, perioral tingling and numbness, Trousseau's sign, prolonged QT

Hypermagnesemia: S&S, treatment

Causes lethargic state; usually in renal failure patients taking supplements. Tx: calcium

Hypomagnesemia: S&S

Usually occurs with massive diuresis, chronic TPN without mineral replacement or ETOH abuse; signs similar to hypocalcemia

Calculate anion gap

Na = (HCO3 + Cl) Normal:

DDx: high anion gap acidosis

MUDPILES Methanol, uremeia, DKA, paraldehydes, isoniazid, lactic acidosis, ethylene glycol, salicylates

Acidosis usually secondary to loss of Na/HCO3- (ileostomies, small bowel fistulas).

Normal anion gap acidosis

Tx: normal anion gap acidosis

Tx: underlying cause, keep pH \> 7.20 with bicarbonate, severely decreased pH can affect myocardial contractility.

Usually a contraction alkalosis

Metabolic alkalosis

Electrolyte changes: nasogastric suction

Hypochloremic, hypokalemic, metabolic alkalosis, and paradoxical aciduria

Pathophysiology: electrolyte changes nasogastric suction

- Low Cl/H: NGT suction (hypochloremia, alkalosis) - Low H2O: kidneys reabsorb Na in exchange for K, (Na/K ATPase) thus losing K (hypokalemia) - Na/H exchange to reabsorb H2O with K/H to reabsorb K -\> paradoxical aciduria

Tx: electrolyte disturbance s/t nasogastric suction

Normal saline (need to correct the Cl- deficit)

Time: respiratory compensation

Minutes (CO2 regulation)

Time: renal compensation

Hours-days (HCO3- regulation)

Best test for azotemia

FeNa

Calculation: FeNa

(urine Na/Cr)/(plasma Na/Cr)

Dx: prerenal azotemia - FeNa - Urine Na - BUN/Cr ratio - Urine osomolality

Prerenal azotemia: - FeNa 20 - Urine osmolality \> 500 mOsm

%: renal mass damaged before you see increased Cr and BUN

70% of renal mass must be damaged before you see changes

Prevent renal damage secondary to contrast dyes

Prehydration best prevents renal damage; HCO3- and N-acetylcysteine

Myoglobin and renal toxicity

Converted to ferrihemate in acidic environment, which is toxic to renal cells. Tx: alkalinize urine.

- Release of purines and pyrimidines leads to increased phosphate and uric acid and decreased calcium. - Can result in increased BUN/Cr (from renal damage), EKG changes

Tx: hydration (best), rasburicase (converts uric acid in inactive metabolite allantoin), allopurinol (decreases uric acid production), diuretics, alkalization of urine

Converts uric acid in inactive metabolite allantoin

Rasburicase

Decreases uric acid production

Allopurinol

Vitamin D (cholecalciferol) synthesis

- Made in skin (UV sunlight converts 7-dehydrocholesterol to cholecalciferol) - Goes to liver for (25-OH), then kidney for (1-OH). This creates the active form

Vitamin D: function

Increases calcium-binding protein, leading to increased intestinal calcium absorption

Transporter of iron

Transferrin

Storage form of iron

Ferritin