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F&E final
| Question | Answer |
|---|---|
| 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
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