Flashcards in Fluid and Electrolyte Deck (71):
Sodium level electrolytes
Potassium level electrolytes
Chloride level electrolytes
Bicarbonate (HCO3) electrolytes
Calcium level electrolytes
Phosphorus level electrolytes
Magnesium level electrolytes
sodium, potassium, calcium, magnesium,
chloride, bicarbonate, phosphate, sulfate, proteinate ions
Which electrolyte maintains and regulates the extracellular fluid and body fluid volume?
Which cation far outnumbers any other cation in the ECF?
What are the major electrolytes present in ICF?
Potassium and phosphate
Normal movement of fluid through the capillary walls into tissue is dependent on what type of pressure?
Hydrostatic; the pressure exerted by the fluid on the walls of blood vessels.
The diffusion of water caused by fluid concentration gradient is caused by what?
What causes the ability all of the solutes to have a driving force that promotes water movement between extracellular and intracellular compartments?
Tonicity, which also determines cell size.
What type of pressure determines the amount of hydrostatic pressure needed to stop the flow of water by osmosis?
What causes an increase in urine output due to an increase in the excreation of glucose, mannitol or contrast agents?
What is the natural tendency of a substance to move from an area of high concentration to an area of low concentration?
What causes the movement of water and solutes to move from an area of high hydrostatic pressure to an area of low hydrostatic pressure?
Sodium is higher in ECF, Potassium is higher in ICF, what maintains the balance between these two compartments? Is this mechanism Active or Passive?
The sodium-potassium pump, Active transport.
What is insensible loss?
Fluid loss that is evaporated, not controlled or measured. Water vapor, forming just on the skins surface (respiration, fluid and warmth lost from the lungs).
What is sensible loss?
Fluid excreted by the body that can be felt, seen, and measured. Urination, diarrhea, sweating is an example
What are the 4 organs of fluid loss?
Lungs, skin, kidneys and GI tract
Secretion of this mineralcorticoid causes sodium retention and potassium loss.
What hormone is manufactured by the hypothalamus, stored in the posterior pituitary and released to conserve water in the body?
ADH, antidiuretic hormone.
What corticosteroid is released from the adrenal glad during times of stress that causes sodium and fluid retention?
Which hormone influences calcium absorption in the intestines and reabsorption in the renal tubules?
PTH, Parathyroid Hormone
Decreased respiratory & renal function coupled with decreased muscle mass and fluid deficits can cause what age group to be in danger of fluid and electrolyte imbalance?
Gerontological or elderly, and older adults
What can an excessive volume of IV fluids do to older patients?
Cause fluid overload and cardiac failure
FVD signs and symptoms
Acute weight loss, decreased skin turgor, cap refill time, central venous pressure, and BP; oliguria (decreased urine output), concentrated urine, flattened neck veins, dizziness, weakness, thirst & amp; confusion, nausea, sunken eyes, muscle cramps, increased pulse, cool, clammy, pale skin.
LABS: increased: H/H, BUN, Creatinine, urine specific gravity and osmolarity. Decreased: urine sodium.
What is called when the ratio of water and electrolytes is remains but the fluid volume is deficient?
Hypovolemia or FVD (fluid volume deficit), not be confused with dehydration which is only a water deficit with unbalanced ratio of electrolytes.
What is called when the ratio of water to serum electrolytes remains the same but there is isotonic expansion of the ECF.
Hypervolemia or FVE (fluid volume excess), usually secondary to increased sodium levels.
FVE signs and symptoms
A cute weight gain, peripheral Adema in actives, distended veins, crackle, elevated CVP, shortness of breath, increased BP, respiratory rate, urine output; bounding pulses and cough.
LAB: increased: H/H. Decreased: urine osmolarity, sodium & specific gravity
FVD contributing factors
Lots of water & electrolytes: vomiting, diarrhea, fistulas, fever, excess sweating, burn, blood laugh, GI suction, and third space fluid shift; decreased intake, anorexia, nausea, and the inability to gain access to fluid. Diabetes insipidus and uncontrolled diabetes both contribute to the completion of EFV
FVE contributing factors
Compromised regulatory mechanisms: kidney injury, heart failure; fluid shift from burns. Prolonged corticosteroid therapy, severe stress and hyperaldosteronism.
a type of edema in which fluid accumulates in the peritoneal cavity. Sometimes from cirrhosis or malignant tumors.
Sodium restriction, avoid OTC medications w/o checking first w/ care provider. If retention continues, test home water, a softener may be needed.
I&O every 8 hrs, daily weight, parenteral and oral fluids, and assess mucosa turgor and mental status. Determin the source of fluid loss and take action. If patient is losing fluid via diarrhea, administration of antidiarrheal may be necessary.
Syndrome of Inappropriate Secreation of Antidiuretic Hormone (SIADH) causes
Over secretion of Arginine vasopressin or AVP(released from posterior pituitary), AIDS patients on mechanical ventilation or taking SSRIs should use caution.
Clinical manifestations of hyponatremia
Poor skin turgor, dry mucosa, headache, decreased saliva production, orthostatic hypotension, nausea, vomiting, and abdominal cramping. Neurological: altered mental status, epilepticus, coma due to cellular swelling and cerebral edema.
Clinical manifestation of hypernatrimia
Dehydration, changes in mental status and behavior in older patients, slightly increased body temperature, and thirst. These patients are the very old, very young, have impaired mental status, nephrogenic or have diabetes insipidus.
A deficit in total potassium, when a patient is alkolotic and the potassium shifts to the IFC. Often occurs in patients with potassium-losing diuretics (thiazide & loop diuretics) as well as sodium penicillin and corticosteroids. Loss can also occur due to vomiting or GI suction, the kidneys response is metabolic alkalosis.
Clinical manifestations of Hypokalemia
Flat or inverted (or both) T-waves, depressed ST segments, elevated U wave on ECG. Metabolic alkalosis, and digitalis toxicity.
Evident in older patient due to decreased renin and aldosterone, decreased renal excretion of potassium. Sometimes seen in undiagnosed kidney injury, can be associated with infection, excessive nutritional intake, hyperaldosteronism, Addison disease (sodium loss and potassium retention).
Clinical manifestation of hyperkalemia
Muscle weakness, tachycardia → bradycardia, dysrhythmias, flaccid paralysis, paresthesias, intestinal colic, cramps, abdominal distention, irritability, anxiety.
As total potassium rises cardiac conduction disturbances occur: ECG: tall tented T waves, prolonged PR interval and QRS duration, absent P waves, ST depression
Older patients and those that spend increased time in bed (causing increased bone absorption) are at increased risk. Inflammation of the pancreas can cause increased break down of proteins and lipids as well as excessive secretion of glucagon and potentially causing increased secreation of calcitonin.
Clinical manifestation of hypocalcemia
Tetany, increased neural excitability (also seen in hypomagnesmia), magnesium deficiency, pancreatitis, blood coagulation problems. Numbness, tingling in fingers, toes, and circumoral region; seizures hyperactive deep tendon reflexes, irritability, bronchospasm, anxiety, impaired clotting time, diarrhea, decreased blood pressure and prothrombin. Blood Alkalosis. Chvostek (contraction of facial muscles due to tap of facial nerve in front of ear), Trousseau sign (carpopedal spasm, collection of fingers into a cone shape after BP is inflated)
Clinical manifestation of hypercalcemia
Muscle weakness, constipation, anorexia, nausea and vomiting, polyuria and polydipsia, dehydration, hypo active deep tendon reflexes, lethargy, deep bone pain, pathologic fractures, flank pain, calcium stones, hypertension .
Mortality rate 50% if not treated. Common causes are malignantcies and hyperparathyroidism. Reduces neuromuscular excitability, it suppresses the myoneural junction. It aggravates digitalis toxicity. Emergency treatment with calcitonin.
Thiazides diuretics can cause a slight elevation in Ca.
Loss occurs in the GI tract due to nasogastric suction (low concentration of Mg), diarrhea or fistulas (high concentration of Mg). Occurs w/ alcohol withdrawal, parentral and tube feedings.
Clinical manifestation of hypomagnesemia
Increased neural excitability (also seen in hypocalcemia), Neuromuscular irritability, insomnia, mood changes, anorexia, vomiting, increased tendon reflexes and increase blood pressure. ECG: P VCS, flat or inverted T waves, depressed ST segment, prolonged PR interval, and widened QRS. Neuromuscular irritability, insomnia, mood changes, anorexia, vomiting, increased tendon reflexes and increase blood pressure. ECG: P VCS, flat or inverted T-wave games, depressed ST segment, prolonged PR interval, and widened QRS.
Clinical manifestation of hypermagnesmia
Flashing, hypotension, muscle weakness, drowsiness, hypo active reflexes, depressed respirations, cardiac arrest and coma, diaphoresis. EcG: tachycardia to break the Cartia bradycardia, prolonged PR intervals and the QRS, Pete T waves.Flashing, hypotension, muscle weakness, drowsiness, hypo active reflexes, depressed respirations, cardiac arrest and coma, diaphoresis. ECG: tachycardia —> bradycardia, prolonged PR intervals and QRS, peaked T-waves. Depressed CNS and peripheral neuromuscular junctions.
This is rare due to kidney efficiency with excretion of Mg. Can occur in patient with untreated DKA, hypothyroidism, also a falsely high when blood is drawn from an extremity where the tourniquet was applied too tightly.
Clinical manifestation of hypophosphatemia
Muscle weakness, bone pain & tenderness, paresthesia, chest pain, confusion, cardiomyopathy, respiratory failure, seizures, tissue hypoxia, and susceptibility to infection, nystagmus. Deficiency in ATP therefore impairing oxygen delivery causing neurological manifestations. Hypoxia leads to increased respiratory rate and respiratory alkalosis and acute rhabdomyolysis.
Serum potassium fluid shift to ICF, increased urination or decreased GI absorption of potassium. It can also occur due to heat stroke, prolonged hyperventilation, alcohol withdrawal, malnutrition, DKA, hepatic encephalopathy, and major thermal burns. Respiratory alkalosis can cause a decrease of Phosphorus due to ICF shift.
Tetany, tachycardia, anorexia, nausea and vomiting, muscle weakness, signs and symptoms of hypocalcemia; hyperactive reflexes; soft tissue calcification in lungs, heart, kidneys and the cornea.
Clincal manifestation of Hyperphophatemia
Common in kidney injury. Soft tissue calcification, reduced GFR, decreased urine output, impaired vision and palpitations.
Occurs in GI suctioning, surgery drainage, severe vomiting and diarrhea, as well as metabolic alkalosis.
Administration of aldosterone, ACTH, corticosteroids, bicarbonate or laxatives also decrease levels.
Clinical manifestation of hypochloremia
Agitation, irritability, tremors, muscle cramps, hyperactive deep tendon reflex is, hypertonicity, text me, slow shallow respirations, seizures, dysrhythmias, coma. Labs: decreased serum chloride, sodium, potassium. Increase pH, bicarbonate, carbon dioxide.
Clinical manifestation of hyperchloremia
Tachypnea, lethargy, weakness, deep rapid respirations, decline in cognitive status, decreased cardiac output, dyspnea, tachycardia, edema, dysrhythmias, coma. Labs: increased serum chloride, potassium, urinary chloride level. Decreased serum pH, bicarbonate. Normal anion gap
Metabolic acidosis, due to excessive administration of chloride relative to sodium. It can also occur in bicarbonate ion loss in the kidney or increase of chloride ions in GI tract causing an accumulation of acidifying salts, acidosis occurs. Head trauma, increased perspiration, excess adrenalcorticostroid hormone production, and decreased GFR can also lead to high serum levels
Metabolic Acidosis clinical manifestation
headache, confusion, drowsiness, increased respiratory rate and depth, nausea and vomiting. Hyperkalemia, dysrhythmias and increased potassium.
HCO3 less than 22 mEq/L
pH less than 7.35
Metabolic Alkalosis clinical manifestation
Primarily manifested by symptoms related to decreased calcium ionization, tingling in fingers and toes, dizziness, and hypertonic muscles, neuromuscular activity, atrial tachycardia, depressed respirations, motility and paralytic ileus.
HCO3 greater than 26 mEq/L
pH greater than 7.45
Respiratory acidosis clinical manifestation
Inadequate excretion of CO2, inadequate ventilation, elevated plasma CO2 concentrations, increased levels of carbonic acid.
Acute manifestations: pulmonary edema, aspirations, atelectasis, pneumothorax, ARDS, overdose of sedatives, increased BP, mental cloudiness, confusion and feeling of fullness in the head along with decreased level of consciousness.
Nonemergent: sleep apnea associated with morbid obesity. Occurs in patients with impaired respiratory muscles, MS, Myasthenia Gravis, Guillain-Barré syndrome.
PCO2 greater than 42 mmHg
pH less than 7.35
Respiratory alkalosis clinical manifestation
Anxiety, hypoxemia, early with elite intoxication, gram-negative bacteremia, and inappropriate ventilator settings. Often caused by chronic hepatic insufficiency and cerebral tumors. Lightheadedness due to vasoconstriction and decreased cerebral blood flow, inability to concentrate, numbness in tingling from decreased calcium ionization, tinnitus, and sometimes loss of consciousness. Cardiac affects included tachycardia and ventricular and atrial dysrhythmia
PCO2 is less than 38 mmHg
pH is above 7.45
Replace cellular fluids (hypotonic compared to plasma)