Fluid And Electrolyte

Question 0

Normal osmolality

Answer 0

275-295- normal

295 water deficit

Question 1

Osmolarity

Answer 1

Measures osmotic force of solute per unit of weight of solvent
Solvent-water
Solutes-3 main- NA, glucose, urea

Question 2

Osmolality, cells affected by osmolality of fluid around them

Answer 2

Isotonic- same osmolality - no effect on cell

Hypotonic- more h20 than cell ( less concentrated)- water moves into cells- cells swell- hippo

Hypertonic- less h20 than cell( more concentrated)- water moves out of cells

Question 3

Regulatory mechanisms for f&e

Answer 3

Adrenal glands- secrete aldosterone
Secretion stimulated by increase in plasma k+ and decrease in plasma NA+

Aldosterone works on kidneys to retain sodium and excrete potassium.
Water follows sodium

Question 4

Specific gravity of urine

Answer 4

Readings greater than 1.025 indicate concentrated urine-fvd

Less than 1.010 indicate dilute urine fve

Question 5

Fluid volume excess- pulse is full and bounding

Answer 5

Also causes distended neck veins and increased blood pressure.

Question 6

Volume deficit

Answer 6

Mild to moderate fluid deficit: Compensatory mechanism include sympathetic nervous system stimulation of the heart and peripheral vasoconstriction. Stimulation of heart increased heart rate and, maintains bp in normal limits. Orrhostatic hypotension is common.

Question 7

Sever fluid volume deficit

Answer 7

Causes a weak, threads pulse that is easily obliterated as well as flattened neck veins. Severe untreated fluid deficit will result in shock.

Question 8

Medications that can lead to hypernatremia

Answer 8

IV fluids: hypertonic nacl, excessive isotonic NaCl, IV sodium bicarbonate. Hypertonic tube feelings without water supplements.
Near drowning in salt water.

Question 9

Other causes for hypernatremia

Answer 9

Insensible water loss, osmotic diuretic therapy, diarrhea.

Diseases: diabetes insipidus, primary hyperaldosteronism, crushing syndrome, uncontrolled diabetes mellitus.

Question 10

Treatment for hypernatremia.

Answer 10

Water placement must be provided. If oral fluids cannot be ingested, IV solutions of 5% dextrose in water or hypotonic saline may be given initially. Serum levels must be reduced gradually to prevent too rapid a shift of water back into cells. Overly rapid correction can result in cerebral edema. The risk is greatest in patient who has developed hypernatremia over several days or longer.

Question 11

Treatment of hypernatremia

Answer 11

Goal is to dilute the sodium concentration with sodium- free IV fluids, such as 5% dextrose in water, and to promote excretion of the excess sodium by administering diuretics. Dietary sodium intake will be restricted.

Question 12

Clinical manifestations of hypernatremia with decreased ECF volume

Answer 12

Restlessness, agitation, twitching, seizures, coma
Intense thirst, dry, swollen tongue, sticky mucous membranes, postural hypotension, weight loss, weakness, lethargy
Decreased central venous pressure

Question 13

Hypernatremia with normal

/increased ECF volume

Answer 13

Restlessness, agitation, twitching, seizures, coma

Intense thirst, flushed skin, weight gain, peripheral and pulmonary edema, increased BP and CVP

Question 14

Medications that can cause hyponatremia

Answer 14

Inappropriate use of sodium-free or hypotonic IV fluids. This may occur in patients after surgery or major trauma, during administration of fluids in patients with renal failure, or in patients with psychiatric disorders associated with excessive water intake. SIADH will result in dilutional hyponatremia caused by abnormal retention of water.

Question 15

Clinical manifestations of hyponatremia with decreased ECF volume

Answer 15

Irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma
Dry mucous membranes, postural hypotension, decreased CVP, decreased jugular veing filling, thready pulse, cold and clammy skin.

Question 16

Hyponatremia with normal/increased ECF volume

Answer 16

Headache, apathy, confusion, muscle spasms, seizures, coma, nausea, vomiting, diarrhea, abdominal cramps, weight gain, increased BP and CVP

Question 17

Central diabetes insipidus

Answer 17

A deficiency in they synthesis or release of ADH from the posterior pituitary gland

Question 18

Nephrogenic diabetes insipidus

Answer 18

Decrease in kidney responsiveness to ADH, can result in profound diuretics, thus producing a water deficit and hypernatremia, for both central and nephrogenic.

Question 19

Treatment for hyponatremia

Answer 19

Fluid restriction. If severe symptoms (seizures) develop, small amounts of IV hypertonic saline solution (3%NaCL) are given to restore the serum sodium level in body while the body is returning to a normal water balance.

Question 20

Treatment for hyponatremia cont.

Answer 20

Drugs that block the activity of ADH (aka vasopressin), are used in the treatment of hyponatremia. Conivaptan (vaprisol) results in increased urine output without loss of electrolytes such as sodium and potassium. It should not be used in patients with hypovolemic hyponatremia. Tolvaptan (samsca) is used to treat hyponatremia associated with heart failure, liver cirrhosis, and with SIADH.

Question 21

Hypertonic solutions (3% NaCl)

Answer 21

Require frequent monitoring of BP, lung sounds, and serum sodium levels and should be used in cation because of the risk for intravascular fluid volume excess.,

Question 22

Hyperkalemia > 5.0

Signs and effects

Answer 22

Irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, parasthesias, irregular pulse, cardiac arrest if hyperkalemia is sudden or severe.

ECG changes, tall, peaked t wave, prolonged PR interval, st segment depression, loss of P wave, widening QRS, ventricular fibrillation, ventricular standstill

Question 23

Causes of hyperkalemia

Answer 23

Impaired renal excretion, shift of pot from ICF to ECF, or a combination of these factors. The most common cause of hyperkalemia is renal failure. Hyperkalemia is common in patients with massive cell,destruction.

Metabolic acidosis is associated,with a shift of pot. Ions from ICF to ECF as hydrogen ions move into the cell.

Certain meds: pot- sparring diuretics, ace inhibitors, these drugs reduce kidneys ability to excrete drug.,

Question 24

Treatment for hyperkalemia

Answer 24

Increase elimination of potassium. This is accomplished via diuretics, dialysis, and use of ion-exchange resins such as kayexalate. Force potassium from ECF to ICF, by administering IV insulin along with glucose so patient does not become hypoglycemia or via administration of sodium bicarbonate in the correction of acidosis.

Question 25

Sever hyperkalemia treatment

Answer 25

If patient is experiencing dangerous cardiac dysarthrias, they should receive IV calcium gluconate immediately while the potassium is being eliminated and forced into cells. Hemodialysis is an effective means of removing potassium from the body in a patient with renal failure.

Question 26

Hypokalemia

Answer 26

Can result from a shift of potassium from ECF to ICF. Most common causes are abnormal losses, via kidneys or the GI tract. This occurs when the patient is diuresing, particularly in the patient with elevated aldosterone level. Aldosterone is released when the circulating blood volume is low., it causes sodium retention in the kidneys but loss of potassium in the urine. Magnesium deficiency may contribute to the development of,potassium depletion. Low plasma magnesium stimulates renin release,and subsequent increased aldosterone levels, which results in potassium excretion.,

Question 27

Metabolic alkalosis and potassium

Answer 27

Can cause a shift of potassium into cells in exchange for hydrogen, thus lowering potassium in the ECF.

Question 28

Clinical manifestations of hypokalemia

Answer 28

Hypokalemia alters the resting membrane potential. It is most commonly associated with hyper polarization, or increased negative charge within the cell. This causes reduced excitability of cells. The most serious problem is cardiac. Cardiac changes include impaired repolarization, resulting in flattening of the t wave. The incidence of potentially lethal ventricular dysrhythmias is increased in hypokalemia.

Question 29

Hypokalemia

Answer 29

Patients at risk for hypokalemia and those who are critically ill should have cardiac monitoring to detect cardiac changes related to potassium imbalances. Patients taking digoxin experience increased digoxin toxicity if their serum pot is low. Severe hypokalemia can lead to shallow respirations and resp arrest.

Question 30

Hypokalemia treatment

Answer 30

Treated by giving potassium chloride supplements and increasing dietary intake of potassium. Can be given IV or PO. Except in severe dificiencies,mKCL is never given unless there is ursine output of at least 0.5 ml/kg of body weight per hour.

Question 31

Calcium has an inverse relationship with?

Answer 31

Phosphorus. When phosphorus levels fall, calcium rises, and vice versa.

Question 32

Signs of hypercalcemia

Answer 32

Lethargy, headache, weakness, muscle flaccidity, heart block, anorexia, nausea, vomiting.

Question 33

Signs of hypocalcemia

Answer 33

Facial spasms, muscle tremors, paresthesia