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T2: F&E

Chapter 17 F& E

QuestionAnswer
Cations positively charged
anion negatively charged
Example of cations sodium (Na), potassium (K), calcium (Ca), and magnesium (Mg)
Examples of anions bicarbonate (HCO3), chloride (Cl), and phosphate (PO4)
Prevalent cation in intracellular fluid (ICF). potassium (K)
Prevalent anion in ICF. phosphate (PO4)
Prevalent cation in extracellular fluid (ECF). sodium (Na)
Prevalent anion in ECF. chloride (Cl)
bicarbonate (HCO3) level 22-26 mEq/L
Chloride (Cl) level 96-106 mEq/L
Phosphate (PO4) level 2.4-4.4 mg/dL
Potassium (K) level 3.5-5.0 mEq/L
Magnesium (Mg) level 1.5-2.5 mEq/L
Sodium (Na) level 135-145 mEq/L
Total Calcium (Ca) level 8.6-10.2 mg/dL
Ionized Ca level 4.6-5.3 mg/dL
Movement of molecules from an area of high concentration to one of low concentration. simple diffusion
Uses a protein carrier in the cell membrane to move molecules. facilitated diffusion
Example of facilitated diffusion. glucose transport into the cell.
Uses external energy to move molecules against the concentration gradient - from an area of low concentration to an area of high concentration. active transport
Example of active transport. sodium-potassium pump - ATP is used to move sodium out of the cell and potassium into the cell
The movement of water through a semipermeable membrane that does not allow solutes to cross. osmosis
How does the water move in osmosis? Water moves from the less concentration side (has more water) to the more concentrated side (has less water). This requires no energy.
When does osmosis stop? When the concentration differences disappear or hydrostatis pressure builds sufficiently to oppose any further movement of water.
Amount of pressure required to stop osmotic flow of water. Determined by concentration of solutes in solution. osmotic pressure
Fluids with the same osmolality, or tonicity, as the cell interior. There is no fluid movement with these fluids. isotonic
Solutions in which the solutes are less concentrated than the cells are called. hypotonic (hypoosmolar)
Solutions in which solutes are more concentrated than the cells are called. hypertonic (hyperosmolar)
What happens to red blood cells in isotonic fluids? there is no impact on the RBC
What happens to RBCs if they are surrounded by hypotonic fluid? Water moves into the cell, causing it to swell and possibly to burst.
What happens to RBCs if they are surrounded by hypertonic fluid? Water leaves the cell to dilute the ECF; the cell shrinks and eventually may die.
The blood pressure generated by the contraction of the heart. hydrostatic pressure
What does hydrostatic pressure do at the capillary level? Is the major force that pushes water out of the vascular system and into the interstitial space.
The osmotic pressure caused by plasma colloids in solution. The plasma protein molecules attract water, pulling fluid from the tissue space to the vascular space. oncotic pressure aka colloidal osmotic pressure
The distribution of body water. fluid spacing
The normal distribution of fluid in the ICF and ECF compartments. first spacing
An abnormal accumulation of interstitial fluid (i.e. edema). second spacing
When fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ECF. The fluid is trapped and unavailable for functional use. (i.e. ascites) third spacing
These in the hypothalamus sense a body fluid deficit or increase in plasma osmolality, which stimulates first and antidiuretic hormone release (ADH). osmoreceptors
ADH is also called? vasopressin
Where is ADH synthesized? hypothalamus
Where is ADH stored? posterior pituitary
What is the action of ADH? Acts in the renal distal and collecting tubules causing water reabsorption.
If the plasma osmolality is decreased or there is water excess, what happens to ADH? Secretion of ADH is suppressed, resulting in urinary excretion of water.
These are secreted by the adrenal cortex and help regulate both water and electrolytes. glucocorticoids and mineralocorticoids
What is the primary effect of glucocorticoids (e.g. cortisol)? Have an anti-inflammatory effect and increase serum glucose levels.
Example of mineralocorticoids. aldosterone
What is the function of mineralocorticoids (aldosterone)? Causes sodium retention and potassium excretion. Water is retained with sodium.
Decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule activates what? the renin-angiotensin-aldosterone system (RAAS)
What results due to the activation of the RAAS? aldersterone is secreted
What else can stimulate the release of aldosterone? Increased serum potassium, decreased serum sodium, and release of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland.
These are hormones produced by cardiomyocytes. natriuretic peptides - ANP and BNP
Natriuretic peptides are natural antagonists to the RAAS and are produced in response to what? Increased atrial pressure and high serum sodium levels.
What is the function of natriuretic peptides? They suppress secretion of aldosterone, renin, and ADH, and the action of angiotensin II.
What is the function of natriuretic peptides in the renal tubules? They promote excretion of sodium and water, resulting in a decrease blood volume and pressure.
The invisible vaporization from the lungs and skin that helps regulate body temperature. insensible water loss
How much insensible water is lost in a day? normally about 600-900 mL/day
In older adults structural changes to the kidney and a decrease in the renal blood flow lead to what? A decrease in GFR, decrease in creatinine clearance, and the loss of ability to concentrate urine and conserve water.
What are some hormonal changes that can occur in older adults? A decrease in renin and aldosterone, and an increase in ADH and ANP.
What are some electrolytes that can be lost or become imbalanced due to NG suction? Na, K, H, and Cl
Abnormal loss of normal body fluids, inadequate intake, or plasma-to-interstitial fluid shift. ECF volume deficit (hypovolemia)
Causes of fluid volume deficit. Inc. insensible water loss or perspiration (high fever, heatstroke); DI; osmotic diuresis; hemorrhage; GI losses: vomiting, NG suction, diarrhea, fistula drainage; overuse of diuretics; inadequate fluid intake; 3rd space shifts: burns, intestinal obstruct
Clinical manifestations of hypovolemia. Restless, drowsy, lethargy, confusion, thirst, dry mucous membranes, decreased skin turgor, dec cap refill, postural hypotension, inc pulse, dec CVP, dec UO, inc RR, weak, dizzy, weight loss, seizures, coma
Causes of ECF volume excess (hypervolemia). Excess isotonic or hypotonic IV fluids, HF, renal failure, primary polydipsia, SIADH, Cushing syndrome, long term use of corticosteroids.
Clinical manifestations of hypervolemia. Headache, confusion, lethargy, per. edema, JVD, bounding pulse, inc BP, inc CVP, polyuria (w/normal renal function), dyspnea, crackles, pulm. edema, muscle spasms, weight gain, seizures, coma
This solution is usually given to replace both water and any needed electrolytes. Lactated Ringer's
This solution is used when rapid volume replacement is indicated. isotonic (0.9%) sodium chloride
What is administered when volume loss is a result of blood loss? blood
What is the treatment for hypovolemia? replace water and electrolytes with balanced IV solutions (LR & NS)
What is the treatment for hypervolemia? Remove fluid w/o changing electrolyte composition or osmolality of ECF. Diuretics & fluid restriction are primary forms of therapy, sodium intake restriction.
If fluid excess leads to ascites or pleural effusions what may need to be done? an abdominal paracentesis or thoracentesis
What are some nursing interventions to monitor fluid deficiency or excess? Monitor I&Os, monitor cardiovascular changes; assess resp. status; neurologic changes; daily weights; skin assessment
Urine specific gravity 1.010-1.025
A urine specific gravity that is greater than 1.025 indicates what? concentrated urine
A urine specific gravity that is less than 1.010 indicates what? dilute urine
What are some cardiovascular s/s to watch for with fluid volume excess/deficit? Changes in BP, pulse force, and JVD. Orthostatic hypotension may be evident in patients w/fluid volume deficit.
What are some respiratory changes that may occur w/fluid volume excess? Can result in pulmonary congestion & pulmonary edema as inc hydrostatic pressure forces fluid into the alveoli. The patient will experience SOB & moist crackles on auscultation.
What respiratory changes may occur with fluid volume deficit? Increased respiratory rate as a result of decreased tissue perfusion and resultant hypoxia.
Changes in neurologic function may occur with fluid volume excess/deficit due to what? cerebral edema or reduced cerebral tissue perfusion
When monitoring a patient for any neurologic changes due to fluid volume excess/deficit, what should be assessed? the patient's LOC, pupillary response, and voluntary movement of extremities
Why is it important to monitor the patient's weight with hypervolemia? Should be weighed the same time every day, wearing the same garments, & on the same scale. An increase of 1 kg (2.2 lb) is equal to 1000 mL (1L) of fluid retention (provided the pt has maintained a usual dietary intake or has been NPO)
hypernatremia elevated serum sodium, may occur with water loss or sodium gain
What are some of the causes of hypernatremia? Excess sodium intake, inadequate water loss, disease states
Excessive sodium intake with hypernatremia. IV fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarb; hypertonic tube feedings w/o water supplements; near drowning in salt water
Inadequate water intake with hypernatremia. Can occur if the patient is unconscious or cognitively impaired .
Excessive water loss with hypernatremia (increased sodium concentration). Increased insensible water loss (high fever, heatstroke, prolonged hyperventilation); osmotic diuretic therapy; diarrhea
What are some disease states that can cause hypernatremia? Diabetes Insipidus (DI), primary hyperaldosteronism, Cushing syndrome, uncontrolled diabetes mellitus
What are some clinical manifestations of hypernatremia with decreased ECF volume? restlessness, agitation, twitching, seizures, coma, intense thirst: dry, swollen tongue, sticky mucous membranes, postural hypotension, dec CVP, weight loss, inc pulse, weakness, lethargy
What are some clinical manifestations of hypernatremia with increased ECF volume? restlessness, agitation, twitching, seizures, coma, intense thirst, flushed skin, weight gain, peripheral & pulmonary edema, inc BP, inc CVP
What is the treatment of hypernatremia? Treat the underlying cause. In primary water deficit, fluid replacement orally or IV w/isotonic or hypotonic fluids (D5W, or 0.45% NaCl); if sodium excess dilute the NA conc. w/ D5W & excrete Na w/diuretics, monitor levels & pts response to therapy.
What is the greatest risk for patients who have developed hypernatremia over several days or longer? Quickly reducing serum sodium levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications.
Results from loss of sodium containing fluids and/or from water excess. hyponatremia
What are some common causes of hyponatremia? excessive sodium loss, inadequate sodium intake, excessive water gain (decreased sodium concentration), disease states
Causes for excessive sodium loss. GI losses: diarrhea, vomiting, fistulas, NG suction; Renal losses: diuretics, adrenal insufficiency, Na wasting renal disease; skin losses: burns, wound drainage
Cause for inadequate sodium intake. fasting diets
Cause excessive water gain (decrease sodium concentration) excessive hypotonic IV fluids; primary polydipsia
What are some disease states that can cause hyponatremia? SIADH, heart failure, primary hypoaldosteronism
What are the clinical manifestations of hyponatremia with decreased ECF volume? irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma, dry mucous membranes, postural hypotension, dec CVP, dec jugular venous filling, inc pulse, thready pulse, cold & clammy skin
What are the clinical manifestations of hyponatremia with normal or increased ECF volume? headache, apathy, confusion, muscle spasms, seizures, coma, N/V/D, abdominal cramps, weight gain, inc BP, inc CVP
What are the main s/s of hypernatremia? thirst, lethargy, agitation, seizures, and coma, impaired LOC, symptoms of fluid volume deficit (dec skin turgor, weakness, hypotension)
What are the main s/s of hyponatremia? confusion, irritability, headache, seizures, and coma
What is the treatment for hyponatremia caused by water excess? fluid restriction
If severe symptoms (seizures) occurred in hyponatremia caused by water excess, how would you treat it? Small amoutns of IV hypertonic saline solution (3% NaCl) can restore the serum sodium level while the body is returning to a normal water balance.
How would you treat hyponatremia associated with abnormal fluid loss? fluid replacement with sodium containing solutions
This drug is used in hyponatremia to increase urine output w/o loss of electrolytes such as sodium & potassium. This should not be used in patients w/hyponatremia from excess water loss. conivaptan (Vaprisol)
This drug is used in hyponatremia associated with heart failure, liver cirrhosis, and SIADH. tolvaptan (Samsca)
Drug therapy for hyponatremia involves agents that block the activity of what? ADH (vasopressin)
What is the major ICF cation? potassium
What is potassium used for? Transmission and conduction of nerve and muscle impulses, cellular growth, maintenance of cardiac rhythms, acid-base balance
This maintains the concentration difference by moving potassium into the cell and sodium out. sodium-potassium pump
What functions are commonly affected by potassium imbalances? neuromuscular and cardiac
Potassium is required for this to be deposited in muscle and liver cells. glycogen
What are some good sources of potassium? diet: mainly from fruits, dried fruits, & veggies; salt substitutes, parenteral sources: IV fluids, transfusion of stored, hemolyzed blood, and medications (e.g. potassium penicillin).
What is the primary route for potassium loss? kidneys; eliminate 90% of daily K intake
What type of relationship does sodium and potassium have? inverse
Factors that cause sodium retention (e.g. low blood volume, increased aldosterone level) causes what to happen with potassium? causes potassium loss in the urine
Large urine volumes can be associated with excess loss of this in the urine. potassium
If kidney function is significantly impaired what can happen to the potassium? retained potassium can lead to toxic levels
What is the most common cause of hyperkalemia? renal failure
What are some other causes of hyperkalemia? Adrenal insufficiency: acidosis, massive cell destruction, and exercise can lead to shift of K from ICF to ECF, increasing K levels; digoxin like drugs & beta-adrenergic drugs; potassium sparing diuretics, ARBs, & ACEI
How does adrenal insufficiency lead to retention of K? there is a subsequent aldosterone deficiency
Examples of massive cell destruction that can cause potassium retention. burn or crush injury, tumor lysis, severe infections
In metabolic acidosis, potassium ions shift from the ICF to the ECF in exchange for these moving into the cell. hydrogen ions
How do digoxin like drugs and beta-adrenergic blocking drugs result in a higher ECF potassium concentration? they impair entry of potassium into cells
These drugs may inhibit the development of hyperkalemia by reducing the kidney's ability to excrete potassium. K sparing diuretics (amiloride - Midamor, spironolactone - Aldactone), ARBs, and ACEI (enalapril - Vasotec, lisinopril (Prinivil)
What are some clinical manifestations of hyperkalemia? irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyperkalemia is sudden or severe
What are some ECG changes associated with hyperkalemia? tall, peaked T wave; prolonged PRI; ST segment depression; loss of P wave; widening QRS; Vfib; ventricular standstill
What is the treatment of mild hyperkalemia with functioning kidneys? It may be sufficient to withhold potassium from the diet and IV sources and increase renal elimination by administering fluids and possibly diuretics.
This drug is administered orally or rectally and binds to potassium in exchange for sodium and the resin is excreted in feces. kayexelate
Patients with moderate hyperkalemia should be treated with this to force potassium into the cells. IV insulin and glucose; sodium bicarb if the patient is acidotic
For patients that have significant hyperkalemia, what should they be monitored for? Should be monitored for dysrhythmias and should receive IV calcium gluconate immediately. Monitor BP b/c rapid administration of calcium can cause hypotension.
What are the causes of hypokalemia? Increased loss of K via the kidneys or GI tract (most common); increased shift of K from ECF to ICF; dietary K deficiency (rare); magnesium deficiency; metabolic alkalosis, skin loss: diaphoresis; dialysis
GI tract losses of potassium are associated with? diarrhea, laxative abuse, vomiting, and ileostomy drainage
Renal loss of potassium occur when? the patient has a low magnesium level or is diuresing, particularly in the patient with an elevated aldosterone level (hyperaldosteronism)
This is released when the circulating blood volume is low, causing sodium retention in the kidneys w/a loss of potassium in the urine. aldosterone
Low plasma magnesium stimulates this, which results in potassium excretion. stimulates renin release and subsequent increased aldosterone levels
What are some factors that cause potassium to move from the ECF to the ICF? insulin therapy (esp in conjunction with diabetic ketoacidosis) & beta-adrenergic stimulation (catecholamine release in stress, coronary ischemia delirium tremens, admin of B-agonists)
This can cause a shift of K into cells in exchange for hydrogen, thus lowering the K in the ECF and causing symptomatic hypokalemia. alkalosis
Lack of K intake for hypokalemia include: starvation; diet low in K; failure to include K in parenteral fluids if NPO
Shift of K into cells for hypokalemia include: increased insulin (e.g. IV dextrose load); alkalosis; tissue repair; increase epinephrine (e.g. stress)
What are some clinical manifestations of hypokalemia? fatigue; muscle weakness, leg cramps; N/V, paralytic ileus; soft, flabby muscles; paresthesias, decreased reflexes; weak, irregular pulse; polyuria; hyperglycemia
Hypokalemia alters this, resulting in hyperpolarization (an increased negative charge w/i the cell) and impaired muscle contraction. CM involves changes in cardiac (most important) and muscle function. the resting membrane potential
Skeletal muscle weakness and paralysis may occur with hypokalemia; initially affects what muscles? leg muscles
Severe hypokalemia can cause weakness or paralysis of respiratory muscles which can lead to? shallow respirations and respiratory arrest
How can hyperglycemia occur in hypokalemia? Can impair function in nonmuscle tissue by impairing insulin secretion.
What ECG changes are associated with hypokalemia? ST segment depression; flattened T wave; presence of U wave; prolonged QRS; ventricular dysrhythmias (e.g. PVCs); bradycardia
Treatment of hypokalemia consists of what? Oral or IV KCl supplements and increased dietary intake of K.
Except in severe deficiencies, KCl is not given unless? There is urine output of at least 0.5 mL/kg of body weight per hour
IV KCl must always be _____ and never given in ____ amounts. diluted; concentrated
The rate of IV administration of KCl should not exceed what? 10-20 mEq/hour and must be administered by infusion pump to ensure correct administration rate
Because KCl is irritating to the vein what should be assessed hourly? assess IV sites for phlebitis and infiltration
Infiltration can cause what to the surrounding tissue? necrosis & sloughing
What should be used when rapid correction of hypokalemia is necessary? a central IV line
This is the major cation in the structure of bones and teeth. Calcium (Ca)
What is the function of Ca? formation of teeth and bone; blood clotting; transmission of nerve impulses; myocardial contractions; & muscle contractions
Calcium absorption requires the active form of what? Vitamin D
What is the main source of calcium? dietary intake
What are the sources of Vitamin D? either ingested in the diet or formed in the skin in the presence of sunlight
What are the 3 forms of calcium? free or ionized; bound to protein (primarily albumin); and complexed with phophate, citrate or carbonate
Created by: eblanc1