Fluids And Electrolytes Flashcards

1
Q

effective osmolality or tonicity is

A

2 × [Na+ ] + glucose/18 (normal range, 275 to 290 mOsm/L)

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2
Q

The concentration of Na + does not give information regarding volume status. Therefore, the first step in the evaluation should include

A

clinical evaluation of ECF volume status plus comparing measured and calculated plasma osmolalities

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3
Q

HYPEROSMOLAR HYPONATREMIA common cause

A

(PLASMA OSMOLALITY [POSM ] >295 mOsm/kg H2 O)

This happens commonly with severe h glycemia.

Each 100 milligram/dL increase in plasma glucose above the normal level of 100 milligrams/dL decreases the serum [Na+ ] by 1.6 mEq/L.

Administration of osmotic agents such as mannitol, glycerol, and maltose, causing an osmolar gap and hyponatremia

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4
Q

Syndrome of Inappropriate Secretion of Antidiuretic Hormone Diagnostic Criteria

A
  • Hypotonic hyponatremia with (P OSM <275 mOsm/kg H2 O)
  • Inappropriately elevated urinary osmolality (usually >200 mOsm/kg)
  • Elevated urinary [Na+ ] (typically >20 mEq/L)
  • Clinical euvolemia
  • Normal adrenal, renal, cardiac, hepatic, and thyroid functions
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5
Q

severe neurologic symptoms initial treatment?

A

vomiting, seizures, reduced consciousness, cardiorespiratory arrest

includes infusion of 3% hypertonic saline

Raising serum sodium by 5 mEq/L is typically all that is required to see an improvement in severe neurologic symptoms.

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6
Q

mild or moderate or in chronic hyponatremia

A

the [Na+] correction should be slower than for acute hyponatremia

For chronic hyponatremia [Na+ ], the correction rate should not exceed 6 mEq/24 h in high-risk patients and 12 mEq/24 h in low-risk patients

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7
Q

Rapid correction increases risk for the most dangerous complication

A

the osmotic demyelination syndrome

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8
Q

Hypertonic (3%) saline can be given at a low infusion rate

A

0.5 to 1 mL/kg/h, with frequent [Na+] checks

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9
Q

Treatment of Hyponatremia Symptomatic With Seizures or Coma

A

Step 1 Assess for indication for 3% hypertonic saline: severe symptoms of hyponatremia such as seizures or coma with suspected impending brainstem herniation in setting of acute *or chronic †hyponatremia

Step 2
Infuse 100–150 mL of 3% hypertonic saline IV over 15–20 min

Step 3
Measure serum sodium level after each 3% hypertonic saline infusion

Step 4
Stop infusion when symptoms improve or a target of a 5 mEq/L (range, 4–6 mEq/L) increase in serum sodium concentration is achieved

Step 5
May repeat 150 mL of 3% hypertonic saline up to 3 total doses, or a total of 450 mL IV of 3% hypertonic saline

Step 6
Keep the IV line open with minimal volume of 0.9% normal saline until cause-specific treatment is started. Limit increase in sodium level to no more than 8–12 mEq/L during the first 24 h or 18 mEq/L over 48 h

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10
Q

Risk factors for osmotic demyelination syndrome

A

[Na+] <120 mEq/L, chronic heart failure, alcoholism, cirrhosis, hypokalemia, malnutrition, and treatment with vasopressin antagonists such as tolvaptan.

Symptoms
dysarthria, dysphagia, lethargy, paraparesis or quadriparesis, seizures, and coma

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11
Q

Treatment forovercorrection

A

5% dextrose in water at 3 mL/kg/h, loop diuretics, and desmopressin

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12
Q

Treatment of Hypernatremia

A

Isotonic (0.9%) saline
Use for correction of volume deficits

Etiology-specific therapy
Treat fever with antipyretics, vomiting with antiemetics, and diabetes insipidus with desmopressin (see “Diabetes Insipidus” section)

D5 W or oral free water to replace free water deficit over 2–3 d
In cases of chronic hypernatremia, it is suggested that correcting (lowering) the sodium level should occur at a rate of no more than 0.5 mEq/L/h or 10–12 mEq/24 h

D5 W to replace free water deficit over 1–2 h
Reserved only for those cases where acuity is known to be <6 h and the salt load is known to be lethal (0.75–3.0 grams/kg of body weight).

Hemodialysis
An alternative or as a supplement to D5 W to replace free water deficit in life-threatening acute cases of salt ingestion.

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13
Q

estimated K +deficit in mEq/L

A

estimated K +deficit in mEq/L = (expected serum [K+ ] in mEq/L – measured serum [K+ ] in mEq/L) × ICF (calculated as 40% of total body weight)

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14
Q

Acid-base imbalance plays an important role in critically ill patients: there

A

inverse proportionality between serum pH and [K+], with [K+ ] rising about 0.6 mEq/L for every 0.1 decrease in pH and vice versa, through an exchange between H +and K+

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15
Q

Symptoms of hypokalemia

A

serum concentrations reach 2.5 mEq/L

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16
Q

Causes of Hypokalemia

A

Transcellular shifts
Alkalosis*
Increased plasma insulin (treatment of diabetic ketoacidosis)
β-Adrenergic agonists
Hypokalemic periodic paralysis (congenital)
Thyrotoxic hypokalemic periodic paralysis

Decreased intake
Fasting Alcoholism (worsened by hypomagnesemia) Eating disorders

GI loss
Vomiting* ,
nasogastric suction Diarrhea * (including laxative, enema abuse) Malabsorption Ureterosigmoidostomy Enteric fistula Villous adenoma

Renal loss
Diuretics (carbonic anhydrase inhibitors, loop diuretics, and thiazide-like diuretics)*
Primary hyperaldosteronism Secondary hyperaldosteronism Licorice ingestion
Excessive use of chewing tobacco Renal tubular acidosis
Postobstructive diuresis Osmotic diuresis Bartter’s syndrome (mimics loop diuretic use)
Gitelman’s syndrome (mimics thiazide diuretic use)
Apparent mineralocorticoid excess and related syndromes (Conn’s, Liddle’s) Drugs and toxins (aminoglycosides, echinocandins, carbenicillin, penicillins, amphotericin B, levodopa, lithium, thallium, cesium, barium, toluene, theophylline, chloroquine, steroids, etc.)

Sweat loss
Heavy exercise
Heatstroke
Fever

Other
Hypomagnesemia
Acute leukemia and lymphomas IV hyperalimentation
Recovery from megaloblastic anemia Hypothermia (accidental or induced)

17
Q

useful tool for differential diagnosis

A

transtubular K +g dient = (Urinary K +× POSM)/(U OSM× Plasma K+)

normal values of 8 to 9 mEq/L.

Values <5 mEq/L suggest hyperaldosteronism;

if paralysis is present, values <3 mEq/L suggest hypokalemic periodic paralysis.

A calcium/phosphate ratio >1.7 on a spot urine is 100% sensitive and 96% specific for thyrotoxic hypokalemic periodic paralysis

18
Q

general principles in hypokalemia correction

A
  1. Use potassium chloride and avoid administering K + in glucose solutions, to reduce insulin-induced K + transfer into cells.
  2. Potassium is irritating to the endothelium; adequate dilution is mandatory to prevent pain and phlebitis (maximum recommended [K+ ] in 500 mL of a saline solution is 40 mEq, to be infused in 4 to 6 hours in a peripheral line). If a more aggressive correction is needed, an identical solution can be administered in a second peripheral line. Higher concentrations can be administered through a central line, but infusion rates should never exceed 20 mEq/h.
  3. Reassessing serum [K+ ] should be adjusted to infusion rate and coexisting factors (e.g., concomitant acid-base imbalance, volume depletion, cardiac arrhythmias).
  4. ECG monitoring is recommended.
  5. In most cases, hypokalemic patients are also hypomagnesemic. Thus, magnesium (20 to 60 mEq/24 h) may be added to the infusion both to optimize tubular reuptake of potassium and to contrast proarrhythmic effect of hypokalemia.