Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove Ads
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards




share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

F&E final

QuestionAnswer
Hypervolemia potential causes burns, cirrhosis, hypertonic IV fluids, blood transfusion
S/S of hypervolemia The excess fluid, primarily Na & H2O, builds up in the body,leads increase in weight, peripheral edema, ascites. Eventually, fluid enters air spaces in lungs, reduces amount of O2 that enters blood. Causes sob (dyspnea) & (paroxysmal nocturnal dyspnea)
Hypervolemia is excess fluid in the ICF (blood)
The normal osmolarity value for plasma and other body fluids ranges 270-300 mOsm/L
Osmolality is the number of milliosmoles in a kilogram of solution
Hypertonic >300 mOsm/L lots of particles, low water, high osmotic pressure.
Hypotonic <270 mOsm/L, low osmotic pressure, water is pulled from them, more water than solvent
Water loss from the skin, lungs, and stool is called insensible water loss, because it cannot be controlled
The endocrine system helps control fluid and electrolyte balance. Three hormones that help control these critical balances are aldosterone, antidiuretic hormone (ADH), and natriuretic peptide (NP).
Aldosterone is a hormone secreted by the adrenal cortex whenever sodium level in the extracellular fluid (ECF) is decreased.
Aldosterone prevents both water and sodium loss.
When aldosterone is secreted, it acts on the kidney nephrons, triggering them to reabsorb sodium and water from the urine back into the blood. Increases blood osmolarity and blood volume.
Antidiuretic hormone (ADH), or vasopressin, is produced in the brain and stored in the posterior pituitary gland.
ADH release from the posterior pituitary gland is controlled by the hypothalamus in response to changes in blood osmolarity, specifically blood Na levels
ADH acts directly on kidney tubules and collecting ducts, making them more permeable to water. As a result, more water is reabsorbed by these tubules and returned to the blood, decreasing blood osmolarity by making it more dilute.
creating effects that are opposite of aldosterone ANP & BNP (loss of Na & H20 in urine and decrease of CO and BP, vasodilator
difference between actual and relative actual equals loss and relative is rearranged
Fluid loss from ECF only isotonic dehydration, the most common type
A decrease in circulating blood volume hypovolemic
What is the best indicator of fluid loss or retention changes in weight
S/S of hypovolemia ↑HR, ↓BP, ↑respirations, weak peripheral pulses, difficult to find, and easily blocked with light pressure. Ϫ in mental status, tenting, slight fever, specific gravity>1.030
Usually, laboratory findings with dehydration show elevated levels of hemoglobin, hematocrit, serum osmolarity, glucose, protein,BUN, and various electrolytes.
Management of dehydration aims to prevent injury, prevent further fluid losses, and increase fluid compartment volumes to normal ranges. Main strategies include patient safety, fluid replacement, and drug therapy.
The two most important areas to monitor during rehydration are pulse rate and quality and urine output.
Isotonic saline solution 9% saline (osmolarity 308)
.45% saline hypotonic (154 mOsm/L)
5% dextrose in water (D5W) isotonic (274 mOsm/L)
10% dextrose in water (D10W) hypertonic (500 mOsm/L)
Ringer's lactate isotonic (274 mOsm/L)
5% dextrose in Ringer's lactate hypertonic (500 mOsm/L)
S/S of hypervolemia pitting edema, ↑PR, ↑BP, JVD, wt ↑, ↑resp.rate, moist crackles, HA, blurred vision, cool skin, muscle weakness, specific gravity <1.050
Labs with hypervolemia serum electrolyte values are normal, but decreased hemoglobin, hematocrit, and serum protein levels may result from excessive water in the vascular space (hemodilution).
Complications of hypervolemia pulmonary edema and heart failure
Hypervolemia drug therapy loop diuretics furosemide (Lasix), or potassium sparing conivaptan (Vaprisol)
more than a 3-pound gain in a week or more than a 1- to 2-pound gain in 24 hours indication of fluid retention
function of Na skeletal muscle contraction, cardiac contraction, nerve impulse transmission, and normal osmolarity and volume of the ECF.
Normal Na 135-145 mEq/L
Normal Ca 9.0-10.5 mEq/L
Normal K 3.5-4.5 mEq/L
Normal Cl- 98-106 mEq/L
Normal Mg 1.3-2.1 mEq/L
Normal P 3.5-4 mEq/L
Function of K Regulation of intracellular osmolarity, Maintenance of electrical membrane excitability, Maintenance of plasma acid-base balance
Function of P Activation of B-complex vitamins, Formation of adenosine triphosphate and other high-energy substances, Cofactor in carbohydrate, protein, and lipid metabolism,
Function of Mg Excitable membrane stabilizer, Essential element in cardiac, skeletal, and smooth muscle contraction, Cofactor in blood-clotting cascade, Cofactor in carbohydrate metabolism, Cofactor in DNA and protein synthesis
Function of Cl Maintenance of plasma acid-base balance, Maintenance of plasma electroneutrality, Formation of hydrochloric acid
Function of Ca Cofactor in blood-clotting cascade, Excitable membrane stabilizer, Adds strength/density to bones and teeth, Essential element in cardiac, skeletal, and smooth muscle contraction
Low serum sodium levels inhibit the secretion of ADH and NP and trigger aldosterone secretion. Together these actions increase serum sodium levels by increasing kidney reabsorption of sodium and enhancing kidney loss of water.
High serum sodium levels inhibit aldosterone secretion and directly stimulate secretion of ADH and NP. Together these hormones increase kidney excretion of sodium and kidney reabsorption of water.
With hyponatremia, the osmolarity of the ECF is lower than that of the intracellular fluid (ICF). As a result, water moves into the cell, causing swelling. Even a small amount of swelling can reduce cell function. Larger amounts of swelling can make the cell burst and die (lysis).
ACTUAL SODIUM DEFICITS Excessive diaphoresis • Diuretics (high-ceiling diuretics)• Wound drainage (especially gastrointestinal)• Decreased secretion of aldosterone• Hyperlipidemia • Renal disease (scarred distal convoluted tubule)• Nothing by mouth• Low-salt diet
RELATIVE SODIUM DEFICITS (DILUTION) Excessive ingestion of hypotonic fluids • Psychogenic polydipsia• Freshwater submersion accident• Renal failure (nephrotic syndrome)• Irrigation with hypotonic fluids• Syndrome of inappropriate antidiuretic hormone secretion• Hyperglycemia• Heart failure
S/S of hyponatremia Ϫ in mental status, muscle weakness, ↓ Deep tendon reflexes, ↓BP N/V, diarrhea, ↑GI motility, w/hypovolemia- rapid, weak, thready pulse, w/hypervolemia bounding pulse w/norm or ↑BP
Tx for hyponatremia and hypovolemia IV saline solution or for sever a hypertonic IV solution on a controller
Hyponatremia and hypervolemia Tx mannitol (Osmitrol), or conivaptan (Vaprisol). Assess for K ↓& Na ↑, fluid loss
ACTUAL SODIUM EXCESSES • Hyperaldosteronism • Renal failure• Corticosteroids• Cushing's syndrome or disease • Excessive oral sodium ingestion• Excessive administration of sodium-containing IV fluids
RELATIVE SODIUM EXCESSES • Nothing by mouth• Increased rate of metabolism• Fever •Hyperventilation• Infection• Excessive diaphoresis• Watery diarrhea• Dehydration
when serum sodium levels are high, severe cellular dehydration occurs
SS of hyper natremia Ϫmental status or w/fluid overload-lethargy, muscle twitching, bilateral muscle weakness, ↓deep tendon refex, ↑PR (w/hypovolemia), ↑BP, JVD, bounding PR (w/fluid overload)
Drug therapy is used to restore fluid balance when hyponatremia is caused by fluid loss Hypotonic IV infusions, usually 0.225% or 0.45% sodium chloride
Hypernatremia caused by poor renal excretion of sodium requires drug therapy with diuretics that promote sodium loss, such as furosemide (Lasix, Furoside) or bumetanide (Bumex).
K is highest in meat, fish, and many (but not all) vegetables and fruits.
K is lowest in eggs, bread, and cereal grains
Kidney excretion of potassium is enhanced by aldosterone.
Actual potassium depletion occurs when potassium loss is excessive or when potassium intake is not adequate to match normal potassium loss.
Relative hypokalemia occurs when total body potassium levels are normal but the potassium distribution between fluid spaces is abnormal.
ACTUAL POTASSIUM DEFICITS, Inappropriate or excessive use of drugs •Diuretics •Digitalis •Corticosteroids. Drugs, especially diuretics, corticosteroids, and betaadrenergic agonists or antagonists, can increase potassium loss through the kidney
RELATIVE POTASSIUM DEFICITS • Alkalosis• Hyperinsulinism • Hyperalimentation• Total parenteral nutrition• Water intoxication • IV therapy with potassium-poor solutions
What do you assess first in pt with hypokalemia respiratory
SS of hypokalemia ↓resp. rate, muscle weakness, ↓deep tendon reflex, thready-weak pulses, Ϫmental status, N/V, constipation
Hypokalemia causes ECG changes in the heart, including ST-segment depression, flat or inverted T waves, and increased U waves
Potassium-sparing diuretics include spironolactone (Aldactone, Novo-Spiroton), triamterene (Dyrenium), and amiloride (Midamor).
Loop diuretics and thiazides cause potassium loss
angiotensin-converting enzyme (ACE) inhibitors effects on potassium cause retention of K
ACTUAL POTASSIUM EXCESSES ACE INHB, salt substitute, potassium sparing diuretics Aldacton, Midamor), blood transfusions
RELATIVE POTASSIUM EXCESSES • Tissue damage• Acidosis • Hyperuricemia • Uncontrolled diabetes mellitus
SS of hyperkalemia bradycardia, twitching, weakness, diarrhea, spaztic colon,
Hyperkalemia caused by dehydration, levels of other electrolytes, hematocrit, and hemoglobin also are elevated.
Hyperkalemia caused by renal failure occurs with elevated serum creatinine and blood urea nitrogen, decreased blood pH, and normal or low hematocrit and hemoglobin levels.
How to get K back into the cells with hyperkalemia IV with insulin & glucose (hypertonic)
Absorption of dietary calcium requires the active form of vitamin D.
PTH increases serum calcium levels by releasing free calcium from bone storage sites (bone resorption of calcium), stimulating vitamin D activation to help increase intestinal absorption of dietary calcium, inhibiting kidney calcium excretion, and stimulating kidney calcium reabsorption.
Dietary Management of Hyperkalemia, avoid meats, dried fruit, dairy products and veggies high in K. Eat eggs, bread cereals & canned fruits
ACTUAL CALCIUM DEFICITS Crohn's disease• Inadequate oral intake of calcium• Inadequate intake of vitamin D• End-stage kidney disease• Renal failure—polyuric phase• Diarrhea • Steatorrhea
RELATIVE CALCIUM DEFICITS • Hyperproteinemia• Alkalosis • Calcium chelators or binders• Citrate • Mithramycin• Penicillamine• Sodium cellulose phosphate (Calcibind) • Acute pancreatitis• Hyperphosphatemia • Immobility• Removal/destruction of parathyroid glands
Actual calcium loss (a reduction in total body calcium) occurs when the absorption of calcium from the GI tract slows or when calcium is lost from the body.
Relative calcium loss causes total body calcium amounts to remain normal while serum calcium levels are low. This problem occurs when the unbound calcium in the body is reduced or when parathyroid gland function is decreased.
SS of hypocalcemia CAT charley horses, weak bones, tingling/numbness in hands, tetany, Trousseau's and Chvostek's signs, ↑ abdom sounds/diarrhea
Trousseau’s sign Under hypoxic conditions, a positive Trousseau's sign occurs when the hand and fingers go into spasm in palmar flexion
Chvostek’s signs tap the face just below and in front of the ear (over the facial nerve) to trigger facial twitching of one side of the mouth, nose, and cheek
ACTUAL CALCIUM EXCESSES • Excessive oral intake of calcium• Excessive oral intake of vitamin D • Renal failure• Use of thiazide diuretics
RELATIVE CALCIUM EXCESSES • Hyperparathyroidism, Hyperthyroidism, Immobility• Use of glucocorticoids• Dehydration
The most serious problems with hypercalcemia cardiac, ↑BP &↑ HR at first then ↓with long-term, sever
SS of hypercalcemia altered mental state, ↑BP & HR, muscle weakness, ↓paristalsis, Constipation, anorexia, nausea, vomiting, and abdominal pain are common.
Drug Tx for hypercalcemia phosphorus, calcitonin (Calcimar), bisphosphonates (etidronate), and prostaglandin synthesis inhibitors (aspirin, NSAIDs).
Most P can be found in the bones
Food sources of phosphorus include meats, fish, dairy products, and nuts.
The regulation of ECF phosphorus occurs through the activity of parathyroid hormone (PTH).
Increased PTH levels cause a net loss of phosphorus.
Reduced PTH levels enhance kidney reabsorption of phosphorus, resulting in increased plasma levels of phosphorus.
HYPOPHOSPHATEMIA causes starvation, malnutrition, use of antiacids, respiratory alkalosis, hyperglycemia, DM, renal failure, hypercalcemia, hyperparathyroidism, alcohol
HYPERPHOSPHATEMIA causes • Decreased renal excretion resulting from renal insufficiency• Tumor lysis syndrome • Increased intake of phosphorus• Hypoparathyroidism
SS of hypophosphatemia ↓SV, ↓ CO, ↓PR, generalized muscle weakness, ↓bone density
YOU SHOULD AVOID hypoP Milk, Cheese, Yogurt, Collard greens, Rhubarb
HypoP you should eat Fish, Beef, Chicken, Pork, Organ meats, Nuts, Whole-grain breads and cereals
Causes of increased serum phosphorus levels include renal insufficiency, certain cancer treatments, increased phosphorus intake, and hypoparathyroidism
Normally, magnesium inhibits nerve impulse transmission at synapse areas.
SS of hypoMg ↑deep tendon reflex, Trousseous’s and Chevtkoffs b/c ↓Ca, tetany, confusion, depression, psychosis,. Reduced motility, anorexia, nausea, constipation, and abdominal distention are common.
Tx for hypoMg IV magnesium sulfate (MgSO4)
Magnesium is a membrane stabilizer. When magnesium excess occurs, excitable membranes are less excitable and need a stronger-than-normal stimulus to respond.
SS of hyper Mg bradycardia, peripheral vasodilation, and hypotension, drowsiness, lethargic, coma, reduced or absent deep tendon reflex
Tx for hyperMg loop diuretics & Ca
Bicarbonate (HCO3−) is the anion most commonly exchanged for chloride.
Assess any patient with a fluid or electrolyte imbalance for falls risk.
Assess all patients with hyperkalemia for cardiac dysrhythmias and ECG abnormalities, especially tall T waves, conduction delays, and heart block.
Assess the respiratory status of all patients with hypokalemia
Acid base balance is done through the control and release of H
Normal body pH 7.35-7.45 slightly alkaline
Substances that release H in water are acids
A strong acid release H easily (HCl→H+Cl)
a weak acid, contains a total of four hydrogen molecules. In water it releases on 1 of H
H acceptors are bases. They reduce the amount of free H in a solution
HCo3 is a weak base
Buffers can either release H into a solution or bind it
Carbonic acid(H2Co3) most common acid releases it’s H easily to form bicarb (most common base) 1:20 ratio
Carbohydrate metabolism creates CO2
Protein breakdown creates sulfuric acid
Fat breakdown creates ketoacids and fatty acids
Normal PaCo2 35-45
Normal Bicarb 21-28
Normal PaO2 80-100
Incomplete anaerobic metabolism of glucose lactic acid. Anaerobic conditions occur with hypoxia, sepsis, and shock.
Chemical buffers bicarb and phosphate
The most common buffer in the body is protein buffers albumin and globulin (ECF), hemoglobin (ICF)
Normal line of defense for pH imbalances chemical buffers (bicarb & phosphate), protein buffers (albumin, globulin, hemoglobin), respiratory and renal (slowest to respond)
Renal defenses in pH balance bicarb production and distribution, phosphate elimination and ammonia secretion
Acid is excreted in the urine by bicarb is formed in the kidney, it is reabsorbed into the blood to balance acid level. Phosphate is excreted in the urine and picks up an extra acid (H) to form dihydrogen phosphate ion
Ammonia is excreted in the urine and picks up H to form ammonium
Partially compensated pH close to normal with bicar hi or low (metabolic), O2 hi/low
Fully compensated pH normal with bicarb hi/low, O2 hi/low
Actual acidosis problems that actually increase acid production are diabetic ketoacidosis and seizures or problems that actually decrease acid elimination are respiratory impairment and renal impairment.
In relative acidosis, the amount or strength of acids does not increase. Instead, the amount or strength (or both) of the bases decreases (to create a base deficit), which makes the fluid relatively more acidic than basic.
A relative acidosis (base deficit) is caused by either overeliminating bases (bicarbonate ions [HCO3−]) or underproducing bases.
Examples of problems that underproduce bases are pancreatitis and dehydration (relative)
A condition that overeliminates bases is diarrhea (relative)
SS of acidosis lethargy, confusion, ↓muscle tone & deep tendon reflex, bradycardia, tall T waves, hypotention, thready pulses, Kussmaul resp, warm, flushed skin and cyanosis
Normal bicarb level 21-26. Acid is <21
Normal PaCO2 35-45. Acid is >45
Respiratory acidosis PaO2 ↓, PaCO2↑, pH↓
Serum potassium levels are elevated in acute respiratory acidosis. They are normal or low in chronic respiratory acidosis when renal compensation is present.
Chronic respiratory acidosis is indicated by an elevated bicarbonate level and increased PaCO2.
In an actual base excess, alkalosis occurs when base (usually bicarbonate) is either overproduced or undereliminated.
In relative alkalosis, the actual amount or strength of bases does not increase. Instead, the amount or strength (or both) of the acids decrease, creating an acid deficit and making the blood more basic than acidic.
A relative base-excess alkalosis (acid deficit) results from an overelimination or underproduction of acids
Common causes of metabolic alkalosis Increase in bases:ingesting too much antacids (bicarb)or decrease in acids: NG suctioning, vomiting, Thiazide diuretics
Hyperventilation respiratory alkalosis
Hypocalcemia and hypokalemia occur with alkalosis
SS of alkalosis tetany, dizziness, confusion, Trousseous’s & Chvostek, ↑HR, thready pulse, ↑sensitivity to digoxin, muscle cramps, weakness, ↑respirations
Hypokalemia effects on digoxin toxicity
Chemical buffers are the immediate way that acid-base imbalances are corrected.
Check the serum potassium level for any patient who has acidosis.
Assess heart rate and rhythm for a person with an acid based imbalance at least every 2 hours
Assess the oxygenation status of any patient with acidosis
Normal glucose levels in blood 70-99
Normal Bun levels 7-21
Normal serum Creatinine 0.5 - 1.4(mg/dl) (kidney function)
Normal Creatinine clearance 75-125 ml/dL
Created by: Jillzs