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Fluids and Electrolytes > 02 Body Fluid Changes > Flashcards

02 Body Fluid Changes Flashcards

1
Q

Average intake of water for a healthy person?

A

2000mL of water per day
75% oral intake
25% extracted from solid food

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2
Q

Daily water losses come from?

A

800-1200mL Urine
250mL Stool
600mL Insensible losses (75% skin, 25% lungs)
+ Fever, hypermetabolism, hyperventilation

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3
Q

To clear the products of metabolism, the kidneys must excrete how much urine?

A

A minimum of 500-800mL of urine per day, regardless of the amount of oral intake.

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4
Q

What is the most common fluid disorder in surgical patients?

A

Extracellular volume deficit

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5
Q

Differentiate signs of acute versus chronic ECF volume deficit.

A

Acute volume deficit: CV and CNS signs

Chronic deficits: Tissue signs

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6
Q

The most common cause of volume deficit in surgical patients?

A

Loss of GI fluids

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7
Q

Causes of extracellular volume excess?

A
  1. Iatrogenic
  2. Renal dysfunction
  3. CHF
  4. Cirrhosis

Symptoms are pulmonary and cardiovascular.

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8
Q

Causes of dilutional hyponatremia?

A
  1. Excess oral water intake
  2. Iatrogenic IV excess free water administration
  3. Increased secretion of ADH (postop patients), which increases reabsorption of free water from kidneys, with subsequent volume expansion and hyponatremia.
  4. Antipsychotics, tricyclic antidepressants, ACE inhibitors, which cause water retention, and subsequent hyponatremia.
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9
Q

Causes of depletional hyponatremia?

A
  1. Decreased intake
  2. Increased loss of sodium containing fluids (GI losses, prolonged nasogastric suctioning, diarrhea, renal loss from primary renal disease or diuretics)

There is usually a Concomitant ECF volume deficit.

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10
Q

Causes of hyperosmolar hyponatremia?

A

Excess of solute relative to free water

  • Hyperglycemia
  • Mannitol
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11
Q

Computation for the corrected sodium concentration in hyponatremic, hyperglycemic patients?

A

For every 100mg/dL increment in plasma glucose above normal, plasma sodium should decrease by 1.6mEq/L.

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12
Q

Pseudohyponatremia is caused by?

A

Extreme elevations in plasma lipids and proteins

No true decrease in extracellular sodium relative to water

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13
Q

How to determine cause of hyponatremia?

A
  1. Hyperosmolar causes (pseudohyponatremia, mannitol administration) should be excluded.
  2. Depletional versus dilutional? In the absence of renal disease, depletion is associated with low urine sodium levels <20mEq/L.
    (Renal sodium wasting shows high urine sodium levels)
  3. Dilutional causes are usually associated with hypervolemic circulation.
  4. A normal volume status in the setting of hyponatremia should prompt an evaluation for SIADH.
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14
Q

Hypervolemic hypernatremia is caused by?

A
  1. Iatrogenic administration of sodium-containing fluids (including sodium bicarbonate)
  2. Mineralocorticoid excess (Hyperaldosteronism, Cushing’s syndrome, CAH)
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15
Q

Laboratory findings in hypervolemic hypernatremia?

A
  1. Urine sodium >20 mEq/L

2. Urine osmolarity >300 mOsm/L

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16
Q

Causes of normovolemic hypernatremia?

A
  1. Renal causes (diabetes insipidus, diuretic use, renal disease)
  2. Nonrenal water loss from GI tract or skin
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17
Q

Labs in hypovolemic hypernatremia?

A
  1. Urine sodium <20mEq/L (<15 in nonrenal water loss)

2. Urine osmolarity <300-400 mOsm/L (>400 in nonrenal water loss)

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18
Q

Symptomatic hypernatremia manifests at what sodium level?

A

> 160 mEq/L

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19
Q

Pathophysiology of symptomatic hypernatremia?

A

Water shifts from the ICF to ECF in response to a hyperosmolar extracellular space, resulting in cellular dehydration. This can put traction on the cerebral vessels and lead to SAH.

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20
Q

Classic signs of hypovolemic hypernatremia?

A
  1. Tachycardia
  2. Orthostasis
  3. Hypotension

*Others: Dry, sticky mucous membranes

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21
Q

How much of the total body potassium is in the extracellular compartment?

A

2%

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22
Q

Causes of hyperkalemia?

A
  1. Increased intake (oral/IV supplementation)
  2. Increased release of K+ from cells (Red cell lysis post-BT, rhabdomyolysis, crush injuries, acidosis, hyperglycemia, IV mannitol)
  3. Impaired K+ excretion from kidneys (potassium-sparing diuretics, ACE inhibitors, NSAIDs, acute/chronic renal insufficiency)
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23
Q

Symptoms of hyperkalemia?

A 
GI (nausea, vomiting, intestinal colic, diarrhea)
Weakness, ascending paralysis, respiratory failure
ECG changes (high peaked T waves-- early, widened QRS complex, flattened p wave,  prolonged PR interval-- first degree block,  sine wave formation, ventricular fibrillation), arrhythmia, arrest
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24
Q

Causes of hypokalemia?

A
  1. Inadequate K+ intake
  2. Excessive K+ excretion
  3. K+ loss in pathological GI secretions (Diarrhea, fistulas, vomiting)
  4. Intracellular shifts from metabolic alkalosis or insulin therapy
  5. Drug-induced Mg depletion (amphotericin, aminoglycosides, cisplatin, ifosfamide)
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25
Q

Symptoms of hypokalemia?

A

Failure of normal contractility of GI smooth muscle, skeletal muscle, cardiac muscle: Ileus, constipation, weakness, fatigue, diminished reflexes, paralysis, cardiac arrest.

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26
Q

ECG changes suggestive of hypokalemia?

A

U waves, T wave flattening, ST segment changes, arrhythmias (with digitalis therapy)

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27
Q

How is the change in potassium associated with alkalosis calculated?

A

Potassium decreases by 0.3 mEq/L for every 0.1 increase in pH above normal.

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28
Q

How is serum calcium distributed?

A

Ionized 50%
Protein bound 40%
Complexed to phosphate and other anions 10%

29
Q

How does albumin concentration affect total serum calcium levels?

A

Adjust total serum calcium down by 0.8mg/dL for every 1 g/dL decrease in albumin.

30
Q

Unlike changes in albumin, changes in pH will affect the ionized calcium concentration because?

A

Acidosis decreases protein binding, thereby increasing the ionized fraction of calcium.

31
Q

Define hypercalcemia.

A

Serum calcium level above 8.5-10.5 mEq/L or

An increase in the ionized calcium level above 4.2-4.8mg/dL.

32
Q

Most cases of symptomatic hypercalcemia are caused by?

A

Outpatient: Primary hyperparathyroidism
Inpatient: Malignancy (bony metastasis or secretion of PTH-related protein)

33
Q

Symptoms of hypercalcemia?

A

Neurologic impairment, musculoskeletal weakness/pain, renal dysfunction, nausea, vomiting, abdominal pain, hypertension, cardiac arrhythmias, worsening of digitalis toxicity.

34
Q

ECG changes in hypercalcemia?

A 
Shorted QT interval
Prolonged PR and QRS intervals
Increased QRS voltage
T wave flattening and widening
AV block
35
Q

Define hypocalcemia.

A

Serum calcium level below 8.5mEq/L or

A decrease in the ionized calcium level below 4.2mg/dL

36
Q

Causes of hypocalcemia?

A 
Pancreatitis
Massive soft tissue infections
Renal failure
Pancreatic and small bowel fistulas
Hypoparathyroidism
Toxic Shock Syndrome
Magnesium level abnormalities
Tumor lysis syndrome (Hyperphosphatemia leads to calcium precipitation)
Removal of parathyroid adenocarcinoma (gland atrophy and avid bone remineralization)
37
Q

Cause of asymptomatic hypocalcemia?

A

Hypoproteinemia (results in a normal ionized calcium level)

38
Q

Cause of symptomatic hypocalcemia, with a normal serum calcium level?

A

Alkalosis, which decreases ionized calcium. Neuromuscular and cardiac symptoms do not occur until the ionized fraction falls below 2.5mg/dL (parenthesias of the face and extremities, muscle cramps, carpopedal spasm, stridor tetany, seizures, hyperreflexia)

39
Q

Maneuvers to test for hypocalcemia?

A
  1. Chvostek’s sign: Spasm resulting from tapping over the facial nerve
  2. Trosseau’s sign: Spasm resulting from pressure applied to nerves and vessels of the upper extremity with a blood pressure cuff
40
Q

ECG changes in hypocalcemia?

A

Prolonged QT interval
T-wave inversion
Heart block
Ventricular fibrillation

41
Q

Causes of Hyperphosphatemia?

A
  1. Decreased urinary excretion (impaired renal function, hypoparathyroidism, hyperthyroidism)
  2. Increased intake (IV hyperalimentation solutions, phosphorus-containing laxatives)
  3. Endogenous mobilization of phosphorus (rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe hypothermia, malignant hyperthermia)
42
Q

Causes of hypophosphatemia?

A
  1. Decreased phosphorus intake (malabsorption, administration of phosphate binders, decreased dietary intake from malnutrition)
  2. Intracellular shift of phosphorus (respiratory alkalosis, insulin therapy, refeeding syndrome, hungry bone syndrome)
  3. Increase in phosphorus excretion
43
Q

Causes of hypermagnesemia?

A

Severe renal insufficiency
Parallel changes in potassium excretion
Magnesium-containing laxatives and antacids
Excess intake (TPN, massive trauma, thermal injury, severe acidosis)

44
Q

Symptoms of hypermagnesemia?

A

Nausea, vomiting, neuromuscular dysfunction with weakness, lethargy, hyporeflexia, impaired cardiac conduction leading to hypotension/arrest

45
Q

ECG findings in hypermagnesemia?

A

Increased PR interval
Widened QRS complex
Elevated T waves

46
Q

Causes of hypomagnesemia?

A
  1. Poor intake (starvation, alcoholism, prolonged IV fluid therapy, TPN with inadequate Mg supplementation)
  2. Increased renal excretion (alcohol abuse, diuretic use, amphotericin B administration, primary aldosteronism)
  3. Pathologic losses (GI losses, acute pancreatitis)
47
Q

Symptoms of hypomagnesemia?

A 
Hyperreactive reflexes
Muscle tremors
Tetany
Positive Chvostek's and Trosseau's signs
Delirium and seizures (severe)
Hypocalcemia, persistent hypokalemia
48
Q

ECG changes in hypomagnesemia?

A

Prolonged QT and PR intervals
ST segment depression
Flattening/inversion of P waves
Torsades de pointes

49
Q

How do hydrogen-sensitive chemoreceptors respond to metabolic abnormalities?

A

Acidosis stimulates chemoreceptors to increase ventilation;

Alkalosis decreases activity of chemoreceptors and decreases ventilation.

50
Q

How do the kidneys respond to respiratory abnormalities?

A

The kidneys increase bicarbonate reabsorption in response to respiratory acidosis; and decrease bicarbonate reabsorption in response to respiratory alkalosis.

(Delayed response; hence respiratory acid-base derangements before renal compensation are classified as acute, whereas those persisting after renal compensation are chronic.)

51
Q

Metabolic acidosis results from?

A
  1. Increased intake of acids
  2. Increased generation of acids
  3. Increased loss of bicarbonate
52
Q

The normal anion gap, an index of unmeasured anions, is <12mmol/L. How do you compute for AG?

A

AG = (Na) - (Cl + HCO3)

53
Q

Hypoalbuminemia reduces the anion gap. How to adjust the estimated AG for albumin?

A

Corrected AG = Actual AG - [2.5 (4.5-albumin)]

54
Q

Metabolic acidosis with an increased AG occurs from?

A
  1. Ingestion of exogenous acid (ethylene glycol, salicylates, methanol)
  2. Increased endogenous acid production (Beta-hydroxybutyrate and acetoacetate in ketoacidosis, lactate in lactic acidosis, organic acids in renal insufficiency)
55
Q

Treatment for lactic acidosis?

A

Restore perfusion with volume resuscitation, so lactic acid is rapidly metabolized by the liver and the pH level returns to normal.

56
Q

Why is bicarbonate not always administered in lactic acidosis?

A

Overzealous administration of bicarbonate can lead to metabolic alkalosis, which shifts the oxyhemoglobin dissociation curve to the left. This interferes with oxygen unloading at the tissue level and can be associated with arrhythmias.

Sodium bicarbonate can also exacerbate intracellular acidosis– it can combine with excess hydrogen ions to form carbonic acid, which is then converted to CO2 and water, raising the partial pressure of CO2. This hypercarbia could compound ventilation abnormalities in patients with underlying ARDS. This CO2 can diffuse into cells, but bicarbonate remains extracellular, thus worsening intracellular acidosis.

57
Q

Metabolic acidosis with a normal AG results from?

A
  1. Exogenous acid administration (HCl or NH4+)

2. Loss of bicarbonate (GI disorders, i.e. Diarrhea, fistulas–bicarbonate losses are accompanied by a gain in chloride)

58
Q

How to determine whether the bicarbonate loss has a renal cause?

A

Urinary NH4+ is measured.

Low urinary NH4+ (in hypochloremic acidosis): consider renal tubular acidosis

  • proximal RTA results from decreased tubular reabsorption of HCO3-
  • distal RTA results from decreased acid excretion

Carbonic anhydrase inhibitor Acetazolamide also causes bicarbonate loss from the kidneys.

59
Q

Etiology of increased AG metabolic acidosis?

A

Exogenous acid ingestion: Ethylene glycol, salicylate, methanol

Endogenous acid production: Ketoacidosis, lactic acidosis, renal insufficiency

60
Q

Etiology of normal AG metabolic acidosis?

A 
Acid administration
Bicarbonate loss
GI losses
Ureterosigmoidostomy
Renal tubular acidosis
Carbonic anhydrase inhibitor
61
Q

Etiology of metabolic alkalosis?

A

Increased bicarbonate generation
1. Chloride losing (urinary chloride >20mEq/L)
Mineralocorticoid excess
Profound potassium depletion

  1. Chloride sparing (urinary chloride <20mEq/L)
    Loss from gastric secretions
    Diuretics
3. Excess administration of alkali
Acetate in parenteral nutrition
Citrate in blood transfusion
Antacids
Bicarbonate
Milk-alkali syndrome

Impaired bicarbonate excretion

  1. Decreased glomerular filtration
  2. Increase bicarbonate reabsorption (hypercarbia, potassium depletion)
62
Q

Why are majority of patients with Metabolic Alkalosis hypokalemic?

A

Extracellular potassium ions exchange with intracellular hydrogen ions and allow the hydrogen ions to buffer exces HCO3-.

63
Q

Causes of hypochloremic hypokalemic metabolic alkalosis?

A

Isolated loss of gastric contents in:

  1. Infants with pyloric stenosis
  2. Adults with duodenal ulcer disease

Vomiting with an obstructed pylorus results only in the loss of gastric fluid, which is high in chloride and hydrogen. Hydrogen ion reabsorption eventually ensues, with an accompanied potassium excretion. In response to the associated volume deficit, aldosterone-mediated sodium reabsorption increases potassium excretion. The resulting hypokalemia leads to the excretion of hydrogen ions in the face of alkalosis– a paradoxical aciduria.

64
Q

Treatment for hypochloremic hypokalemic metabolic acidosis?

A

Replacement of fluid deficit with isotonic saline, and then potassium replacement once adequate urine output is achieved.

65
Q

Causes of respiratory acidosis?

A

Hypoventilation caused by:
Narcotics
CNS injury
Pulmonary secretions, atelectasis, mucous plug, pneumonia, pleural effusion
Pain
Limited diaphragmatic excursion due to abdominal pathology

66
Q

Treatment of acute respiratory acidosis?

A

Address underlying cause

Increase ventilation

67
Q

Causes of respiratory alkalosis?

A 
Alveolar hyperventilation from:
Pain
Anxiety
Neurological disorders
Salicylates
Fever
Gram-negative bacteremia
Thyrotoxicosis
Hypoxemia
68
Q

Acute hypocapnia in respiratory alkalosis can lead to?

A

Symptomatic hypokalemia, hypophosphatemia, hypocalcemia with subsequent arrhythmias paresthesias, muscle cramps, seizures

(from uptake of K+ and phosphate into cells and increased binding of calcium to albumin)

69
Q

Treatment of respiratory alkalosis?

A

Direct at underlying cause

Controlled ventilation to address hyperventilation

Fluids and Electrolytes (4 decks)

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