Med Surg Chapter 14-Fluids And Electrolytes

Front 1

Where is body fluid located?

Back 1

2/3 in intracellular fluid
1/3 in extracellular fluid

Front 2

What are the compartments of the ECF?

Back 2

Intravascular- made up of plasma, thrombocytes, erthrocyctes, leukocytes
Interstitial-surrounds cell,ex-lymph
Transcellular-CSF, pericardial, synovial, intraocular, sweat, pleural, digestive

Front 3

What is third spacing?

Back 3

Loss of ECF into a space that does not contribute to equilibrium ICF/ECF (intravascular fluid vol deficit)

Front 4

What causes third spacing?

Back 4

ascites, burns, peritonitis, bowel obstruction, massive bleeding

Front 5

What are the signs/symptoms of third spacing?

Back 5

decreased urine output, decrease BP, increase HR, decrease central venous pressure, edema, increase weight

Front 6

What is milliequivalents?

Back 6

mEq measure of chemical activity, equivalent to 1 g of H+

Front 7

greatest electrolyte in ECF

Back 7

sodium 135-145 mEq/L

Front 8

greatest electrolyte in ICF

Back 8

potassium 3.5-5.0 mEq/L

Front 9

Define osmosis

Back 9

diffusion of water caused by a fluid concentration gradient from area of low solute concentration to high solute concentration

Front 10

Define osmolality

Back 10

concentration of fluid that affects the movement of water between fluid compartments by osmosis
osmoles per kg, concentration of solutes in blood and urine

Front 11

Define osmolarity

Back 11

osmoles per liter of solution, concentration of solutes

Front 12

Define diffusion

Back 12

tendency of substances to move from an area of higher concentration to lower concentration

Front 13

Define filtration

Back 13

movement of water and solutes from an area of high hydrostatic pressure to an area of low hydrostatic pressure

Front 14

Define sodium-potassium pump (active transport)

Back 14

actively moves sodium from the cell into the ECF and potassium into the cell from the ECF (requires energy)

Front 15

Routes of fluid gains and losses

Back 15

urine vol loss= 1-2L/day
sensible and insensible water loss: lungs=300ml/day, skin=600ml/day
GI tract=100-200 ml/day

Front 16

What influences urine osmolality? What is the normal range?

Back 16

urea, creatinine, uric acid
250-900 mOsm/kd
MOST RELIABLE INDICATOR OF URINE CONCENTRATION

Front 17

What causes an increase in urine osmolality?

Back 17

fluid vol deficit, SIADH, CHF, acidosis

Front 18

What causes a decrease in urine osmolality?

Back 18

fluid vol excess, diabetes insipidus, hyponatremia, aldosteronism, pyelonephritis

Front 19

What influences serum osmolality and what is the normal level?

Back 19

glucose, BUN, sodium
275-300 mOsm/kg

Front 20

What causes an increase in serum osmolality?

Back 20

dehydration, water loss, diabetes insipidus, hypernatremia, hyperglycemia, stroke, head injury, renal tubular necrosis, consumption of antifreeze

Front 21

What causes a decrease in serum osmolality?

Back 21

fluid vol excess, SIADH, renal failure, diuretic use, adrenal insuff, hyponatremia, overhydration, paraneoplastic syndrom

Front 22

What does urine specific gravity measure and what is normal?

Back 22

kidney's ability to excrete or conserve water
1.010-1.025

Front 23

What is BUN and the normal value?

Back 23

urea, which is the end product of protein metabolism
(AA breaks down into ammonia which is converted into urea)
10-20 mg/dl

Front 24

What causes an increase in BUN?

Back 24

decreased renal fx, GI bleeding, dehydration, increase protein intake, fever, sepsis

Front 25

What causes a decrease in BUN?

Back 25

end stage live disease, low protein diet, starvation, expanded fluid vol (pregnancy)

Front 26

What is creatinine? Normal Value?

Back 26

end product of muscle metabolism, better indicator of renal fx
0.7-1.4 mg/dl
increases when renal fx decreases (good indicator of reduced renal fx in elderly)
BEST INDICATOR OF RENAL FUNCTION

Front 27

What is hematocrit and what is normal?

Back 27

percentage of RBC in whole blood
W: 35-47% M: 42-52%

Front 28

What increases and decreases hematocrit levels?

Back 28

increase: dehydration and polycythemia
decrease: overhydration and anemia

Front 29

What are normal urine sodium levels, what causes it to increase and decrease, and what can the measurement help diagnose?

Back 29

75-200 mEq/24 h
sodium intake causes increase in excretion, circulating fluid volume increase causes sodium conservation
Helps diagnosis hyponatremia, acute renal failure

Front 30

How do the kidneys help regulate F/E balance?

Back 30

Regulate ECF by: regulating body fluids, unneeded substance, H+, metabolic wates and toxic substances

Front 31

How does the pituitary help regulate fluid balance?

Back 31

hypothalamus makes ADH, which is stored in posterior pituitary gland (controls thirst center)

Front 32

How do adrenal functions regulate fluid balance?

Back 32

Aldosterone (adrenal cortex) causes sodium retention
Cortisol in large quantities produce serum and fluid retention

Front 33

What does the parathyroid hormone do?

Back 33

regulates calcium and phosphate balance

Front 34

What are baroreceptors?

Back 34

small nerve receptors that detect changes in pressure within blood vessels

Front 35

Where are low pressure baroreceptors found?

Back 35

cardiac atria

Front 36

Where are high pressure baroreceptors found?

Back 36

aortic arch, carotid sinues and afferent arterioles

Front 37

What happens when baroreceptors sense a an arterial pressure decrease?

Back 37

less impulses are sent to vasomotor center stimulating the SNS increasing cardiac rate, conduction and contractility, and increase in circulating blood volume
SNS also constricts renal arterioles: increasing release of aldosterone, decreasing GFR, and increases sodium and water reabsorption

Front 38

Describe renin-angiotension-aldosterone system.

Back 38

Decrease in renal perfusion causes a release of renin from kidneys, renin converts angiotensinogen to angiotensin I, angiotensin-converting enzyme converts angiotensin I to II, II causes vasoconstriction, increases arterial perfusion pressure and stimulates thirst, renin causes an increase in aldosterone secretion

Front 39

When is aldosterone released?

Back 39

when serum potassium increases, serum sodium decreases, or adrenocorticotropic hormone increases

Front 40

Where are osmoreceptos located and what do they do?

Back 40

hypothalamus, senses change in sodium concentration

Front 41

Describe how osmoreceptors work?

Back 41

osmotic pressure increases, neurons become dehydrated, posterior pituitary is stimulated to increase release of ADH, ADH travels thru blood to kidneys and causes increased reabsorption of water and decrease urine output

Front 42

What does atrial natriuretic peptide do?

Back 42

released by muscle cells of atria in response to increased cardiac pressure, sympathetic stimulation, vol expansion, hypoxia to decrease blood pressure and volume

Front 43

what causes ANP to decrease and increase?

Back 43

Decrease: chronic heart failure and use of some meds
Increase: acute heart failure, paroxysmal atrial tachycardia, hyperthyroidism, subarachnoid hemorrhage, small cell lung cancer

Front 44

What is normal plasma ANP?

Back 44

20-77 pg/mL

Front 45

Define hypovolemia and how it differs from dehydration?

Back 45

fluid volume deficit- water and electrolytes are lost in the same proportion
dehydration- loss of water alone with increased serum sodium levels

Front 46

What can cause hypovolemia?

Back 46

vomiting, diarrhea, GI suctioning, sweating, decrease intake, diabetes insipidus, adrenal insuff, osmotic diuresis, hemorrhage, coma, third spacing

Front 47

What are the clinic signs of hypovolemia?

Back 47

acute weight loss, decrease skin turgor, oliguria, conc urine, postural hypotension, weak rapid HR, flattened neck veins, increased temp, decreased central venous pressure, cool, clammy skin r/t peripheral vasoconstriction, thirst, anorexia, nausea, lassitude, muscle weakness and cramps

Front 48

What are the diagnotic findings for hypovolemia?

Back 48

increased BUN (relative to creatinine), increased hematocrit level, increased urine specific gravity, increased urine osmolality, hypokalemia (GI and renal losses), hyperkalemia (adrenal insuff), hyponatremia (increased thirst and ADH), hypernatremia (diabetes insipidus, insensible losses)

Front 49

How is hypovolemia treated?

Back 49

-isotonic sol to treat hypotensive patient with FVD
-hypotonic sol once no longer hypotensive

Front 50

What are the nursing assessments for hypovolemic treatment?

Back 50

I/O, weight, central venous pressure, LOC, breath sounds, skin color, tongue turgor, urine specific gravity, decreased peripheral perfusion, decrease body temp, weak rapid pulse

Front 51

What test is used to determine if hypovolemia is caused by reduced renal blood flow or acute tubular necrosis?

Back 51

fluid challenge test, is the renal fuction response normal (increase input, increase output)

Front 52

Describe a fluid challenge test?

Back 52

vols of fluid are given at specific rates and intervals and hemodynatic response is monitored

Front 53

When does shock from hypovolemia occur?

Back 53

when fluid vol loss exceeds 25%

Front 54

How much fluid is lost is there with a 1 lb. weight lost?

Back 54

500 mL

Front 55

Describe isotonic solution normal saline:

Back 55

-0.9% NS (Na 154, Cl 154)
-expands ECF
-used for hypovolemia, shock, diabetic ketoacidosis, metabolic alkalosis, hypercalcemia, mild Na deficit
-mixed with 5% dextrose, becomes hypertonic, 170 cal/L
-only solution given with blood products

Front 56

Describe isontonic solution lactated ringers:

Back 56

-Na 130, K 4, Ca 3, Cl 109 (contains electrolytes in same concentration as plasma)
-used for hypovolemia, burns, fluid lost, acute blood loss replacement
-lactate metabolizes to bicarbonate, do not give if pH>7.5 (alkalosis may result)
-do not use with renal failure (K can cause hyperkalemia)

Front 57

Describe isotonic solution D5W:

Back 57

-5% dextrose in water, no electrolytes
-170 cal/L to aid in renal excretion of solutes
-used for hypernatremia, hypovolemia (not for sole treatment-dilutes plasma), dehydration
-not for head injury (increased ICP), fluid resuscitation (hyperglycemia), cardiac or renal failure (fluid overload), can cause water intoxication and peripheral circulatory collapse

Front 58

Describe hypotonic solution 0.45% NaCl:

Back 58

-Na 77, Cl 77 and free water
-helps kidneys eliminate solutes
-w/ D5% hypertonic 170 cal/L
-used for hypertonic dehydration, Na/Cl depletion, gastric fluid loss
-can cause cv collapse and increased ICP

Front 59

Describe 3% NaCl hypertonic solution:

Back 59

-Na 513, Cl 513
-used to increase EFC vol and decrease cellular swelling (severe hyponatremia)
-must admin slowly

Front 60

Describe 5% NaCl hypertonic solution:

Back 60

-Na 855, Cl 855
-used for severe symptomatic hyponatremia
-admin slowly, no calories

Front 61

Describe colloid solutions:

Back 61

-dextran in NS or 5% D5W (low 40 or high 70)
-used as plasma/vol expander for intravascular ECF
-decreases ability of platelets to clot
-used for hypovolemia in early shock to increase CO, pulse pressure, BP
-not for hemorrhage, thrombocytopenia, renal disease, severe dehydration

Front 62

Define hypervolemia

Back 62

fluid volume excess, caused by abnormal retention of water and sodium (increase total sodium causes increase in water retention, serum sodium stays the same)

Front 63

What causes hypervolemia?

Back 63

fluid overload-- heart failure, renal failure, cirrhosis, excessive intake of sodium

Front 64

What are the s/s of hypervolemia?

Back 64

edema, distended neck veins, crackles, tachycardia, increased BP, pulse pressure and central venous pressure, increased weight, urine output and shortness of breath

Front 65

What are the diagnostic findings for hypervolemia?

Back 65

decreased BUN and hematocrit, low sodium/osmolality levels if kidneys are attempting to excrete excess vol, if aldosterone is stimulated (cirrhosis, HF, nephrotic syndrome) urine sodium levels do not increase

Front 66

How is hypervolemia treated?

Back 66

-diuretics, hemodialysis, sodium restriction

Front 67

Describe the difference between thiazide and loop diuretics:

Back 67

-thiazide- block sodium reabsorption in distal tubules, used for mild-mod hypervol
-loop- block sodium reabsorption in ascending limb of loop of henle, used for severe hypervol

Front 68

What are some of the side effects of diuretics?

Back 68

hypokalemia, hyperkalemia (those with dec renal function), hyponatremia (increased ADH), decreased mag from decreased reabsorptions and increased excretion, azotemia (increases nitrogen levels), high uric acid levels

Front 69

What is the nursing interventions for hypervolemia?

Back 69

I/O, weight, breath sounds, degree of edema, sodium retriction, OTC avoidance, rest, semi-fowlers, turn reg, resp rate, diaphoresis, compression paracentesis, dialysis, elevation of extremeties

Front 70

What is anasarca?

Back 70

severe generalized edema

Front 71

What can cause edema?

Back 71

burns, infections, lymphatic obstruction, decrease in plasma oncotic pressure, HF, renal failure, cirrhosis, nephrotic syndrome

Front 72

What is most abundant electrolyte in the ECF? What is its normal concentration level? How is it regulated? and what does it do?

Back 72

-sodium
-135-145
-ADH, thirst, renin-angiotension-aldosterone system
-necessary for muscle contraction and nerve impulse transmission

Front 73

what is hyponatremia and what causes it?

Back 73

serum sodium < 135, caused by vomiting, diarrhea, fistulas, sweating, diuretics, adrenal insufficiency (aldosterone insuff), dilutional hyponatremia (water intoxication), SIADH

Front 74

What are s/s of hyponatremia?

Back 74

poor skin turgor, dry mucosa, headache, decreased saliva, orthostatic hypotension, nausea, abdominal/muscle cramping, neurological changes (r/t cellular selling and cerebral edema), anorexia, exhaustion

Front 75

What happens when serum sodium levels decrease to <115?

Back 75

increased intracrancial pressure, lethargy, confusion, muscle twitching, focal weakness, hemiparesis, papilledema, SZ

Front 76

What are the clinical findings of hyponatremia?

Back 76

decreased serum osmolality, decrease urine sodium/low specific gravity,

Front 77

How is hyponatremia treated?

Back 77

sodium replacement (LR, isotonic NS), water restriction, small amounts of hypertonic sodium solutions
*water restriction is safest treatment

Front 78

What happens if serum sodium is increased by more than 12 mEq/L in 24 hours?

Back 78

osmotic demylination causes neurological damage

Front 79

What is given with sodium solution to prevent ECF vol overload?

Back 79

loop diuretic

Front 80

What are the nursing interventions for hyponatremia?

Back 80

I/O, weight, serum sodium monitoring, circulatory overload, lithium toxicity (no diuretics), neuro, anorexia, n/v, cramping, lethargy, confusion, muscle twitching, sz

Front 81

What is considered hypernatremia and what can cause it?

Back 81

serum sodium >145
caused by gain of sodium in excess of water- fluid deprivation, hypertonic eternal feedings without adequate water, diabetes insipidus, heat stroke, near death drownding in sea water, hypertonic IV saline solution, excessive use of sodium bicarbonate

Front 82

Physiologically what happens in hypernatremia?

Back 82

water moves out of cell into ECF, cellular dehydration results, increased concetrated ECF is result

Front 83

What are the s/s of hypernatremia?

Back 83

restlessness, weakness, disorientation, delusions, hallucinations, permanent brain damage, dry swollen tongue, flushed skin, edema, postural hypotension, increases reflexes, increased body temp, sz, pulmonary edema, inc HR and BP

Front 84

What are the clinical diagnostics of hypernatremia?

Back 84

serum sodium > 145, serum osmolality >300, urine specific gravity and osmolality are increased

Front 85

How is hypernatremia treated?

Back 85

gradual lowering of serum sodium (0.5-1.0 mEq/L per hour) with hypotonic solution (0.3%NaCl), diuretics or desmopressin for diabetes insipidus

Front 86

What happens if serum sodium is reduced to quickly?

Back 86

fluid goes into brain cells and causes cerebral edema

Front 87

What are the nursing interventions for hypernatremia?

Back 87

I/O, sodium intake, serum sodium levels, thirst, increased body temp, behavior, adequate fluid intake, sufficient water with enteral feedings

Front 88

Where is potassium found, what is the normal value and what does it do?

Back 88

intracellular electrolyte
3.5-5.0
skeletal/cardiac muscle activity

Front 89

What regulates potassium?

Back 89

KIDNEYS excrete 80%
sweat and bowel excrete 20%

Front 90

What is hypokalemia?

Back 90

potassium deficit stores or shirft of serum potassium into cells

Front 91

What causes hypokalemia?

Back 91

diuretics, diarrhea, vomiting, gastric sunctioning, ileostomy, villous adenoma, alkalosis, hyperaldosteronism (causes renal potassium wasting), diuretics, corticosteroids, penicillin, increased insulin, alcoholism, anorexia, bulimia

Front 92

How does hypokalemia cause alkalosis and alkalosis cause hypokalemia?

Back 92

H move out of cell in alkalotic state to correct pH and potassium moves into to the cell to maintain electrically neutral state

Front 93

What are the s/s of hypokalemia?

Back 93

death thru cardiac or resp arrest, fatigue, anorexia, n/v, muscle weakness, leg cramps, decr bowel motility, paresthesias, dysrthymias, increased sensitivity to dig, dilute urine, glucose intolerance, excessive thirst

Front 94

What are the clinical signs of hypokalemia?

Back 94

flat, or inverted T wave, ST depression, elevated U, increase sensitivity to dig toxicity, metabolic alkalosis

Front 95

What is the 24-hour urinary potassium excretion test?

Back 95

distinguishes renal from extrarenal loss
-if urinary potassium excretion exceeds 20mEq/24 hour renal potassium loss is the cause

Front 96

How is hypokalemia treated?

Back 96

diet, oral, IV replacement

Front 97

How does correcting hypokalemia effect the elderly?

Back 97

may retain potassium more readily due to loss of renal function, dig toxicity

Front 98

What are the key points to IV administration of potassium?

Back 98

-never given as a push or IM
-only given in peripheral or central line of 20 mEq/100mL or more requires EKG
-always use infusion pump
-if urine vol decreases to <20 mL/hr for 2 hours stop
-monitor BUN, urine, and creatinine levels

Front 99

What can cause pseudohyperkalemia? Why is this important?

Back 99

tight tourniquet, hemolysis, leukcytosis, throbocytosis
-always retest grossly elevated levels

Front 100

What causes hyperkalemia?

Back 100

decreased renal excression, hypoaldosteronism, addisions disease, meds (heparin, potassium chloride, ACE inhibitors, captorpil, NSAIDS, potassium sparing diuretics)

Front 101

Why should aged (stored) blood not be given to patients with impaired renal function?

Back 101

serum potassium concentration of stored blood increases with time

Front 102

How does acidosis effect hyperkalemia?

Back 102

H moves into cell, potassium moves out into ECF (occurs with burns, major trauma, infections, lysis, etc)

Front 103

What are the s/s of hyperkalemia?

Back 103

tented T, ST depression, shortened QT, prolonged PR and QRS, skeletal muscle weakness, paralysis, nausea, diarrhea, metabolic acidosis

Front 104

How is hyperkalemia treated?

Back 104

dietary potassium restrictions, kayexalate- cation exchange resin, IV calcium gluconate, IV sodium bicarbonate, IV insulin, hypertonic dextrose solution, loop diuretics, peritoneal dialysis, hemodialysis

Front 105

What are the nursing interventions?

Back 105

muscle weakness, dysrthymias, parsthesias, GI symptoms, serum potassium levels, retest is if high, deliver blood quickly, no potassium supplements/potassium sparing diuretics to pts with renal dysfunction, close monitoring of rate and concentration administration

Front 106

Where is most of the body's calcium found and what does it do?

Back 106

skeletal system: bones and teeth
transmission of nerve impulses, regulation of muscle contractions and relaxation, activates enzymes, blood coagulation

Front 107

What is normal serum calcium levels and wht is normal ionized serum calcium levels?

Back 107

Normal serum- 8.6-10.2 mg/dl
ionized- 4.5-5.1 mg/dl

Front 108

How is calcium regulated?

Back 108

as ionized serum calcium decreases parathyroid secretes PTH, increasing calcium absorption
as calcium becomes excessive thyroid gland secretes calcitonin, which inhibits calcium reabsorption from bone and decreases serum calcium concentration

Front 109

What is the result of hypocalcemia?

Back 109

osteoporosis (total body calcium deficit, but serum calcium levels are normal)

Front 110

What can cause hypocalcemia?

Back 110

hypoparathyroidism, massive admistration of citrated blood, pancreatitis (excessive secretion of glucagon causes secretion of calcitonin), renal failure (elevated phosphate levels causes drop in calcium levels), inadequate vit D consumption, magnesium deficiency, medullary thyroid carcinoma, low serum albumin, alkalosis, alcohol abuse

Front 111

What medications can cause hypocalcemia?

Back 111

antacids, amnoglycosides, caffeine, cisplatin, corticosteroids, mithramycin, phosphates, isoniazid, loop diuretics

Front 112

What are the clinical manifestations of hypocalcemia?

Back 112

tetany, tingling, spasms, pain, hyperactive deep tendon reflexes, Trousseau's sign, Chvostek's sign, seizure, depression, impaired memory, delirium, prolonged QT, vent tachycardia (torsades de pointes), dyspnea, largyngospasm

Front 113

What are s/s of chronic hypocalcemia?

Back 113

hyperactive bowel sounds, dry brittle hair, nails and abnormal clotting

Front 114

What is Trousseau's sign?

Back 114

BP cuff 20 over systolic in 2-5 minutes carpal spasm

Front 115

What is Chvostek's sign?

Back 115

tapping 2 cm anterior to earlope results in facial twitching

Front 116

What is the difference between ionized and serum calcium?

Back 116

ionized is free floating in blood, serum is attached to proteins in blood

Front 117

If serum albumin levels are abnormal how does it effect serum calcium levels?

Back 117

interpretation may be off for serum calcium:
Formula to correct: serum ca + (0.8 x 4.0-albumin level)

Front 118

How is hypocalcemia treated?

Back 118

IV admin of calcium slowly, careful with digitalis, diluted in D5W, check for hypotension, infiltration

Front 119

What are nursing management techniques for hypocalcemia?

Back 119

vit D supplementation, Calcium supplementation, weight bearing exercise, avoid antacids, avoid alcohol, caffeine, laxatives, many be given calcium acetate or calcium carbonate antacids to lower phosphate levels before treating hypocalcemia for those with chronic renal failure

Front 120

What is hypercalcemia?

Back 120

excess of calciumin the plasma
-very severe condition, 50% mortality rate

Front 121

What can cause hypercalcemia?

Back 121

malignant tumors cause excessive PTH secretion which releases calcium from bones and increases intestinal and renal absorption of calcium, immobilization (rare), severe or multiple fractures or SCI, thiazide diuretics (potentiate action of PTH- reducing urinary calcium excretion), milk and alkaline antacids, vit D and A intoxication, use of lithium, low phosphorus levels

Front 122

When does calcification of soft tissue occur?

Back 122

when calcium x phosphorus > 70 mg/dl

Front 123

What are the clinical manifestations of hypercalcemia?

Back 123

muscle weakness, incoordination, anorexia, constipation, vomiting, bone pain, abdominal pain, reduced muscle excitability, cardiac standstill (18 mg/dL), digitalis toxicity, excessive urination, severe thirst, confusion, slurred speech, lethargy, psychotic behavior, coma

Front 124

When do severe symptoms of hypercalcemia start to occur?

Back 124

12-16 mg/dL

Front 125

When does hypercalcemic crisis occur and what happens?

Back 125

acute rise in serum calcium level to 17 mg/dL or higher
-thirst, polyuria, nausea, muscle weakness, abdominal cramps, bone pain, cardiac arrest, coma, confusion

Front 126

What are the diagnostic finding for hypercalcemia?

Back 126

serum calcium >10.2
dysrythmias (shortened QT, ST, prolonged PR), osteoporosis, sulkowitch urine test

Front 127

How is hypercalcemia treated?

Back 127

0.9% sodium chloride (dilutes calcium and promotes calcium excretion), IV phosphate, lasix, IM calcitonin (increases urinary excretion), if cancer caused- surgery, chemo, radiation, corticosteriods, bisphosphonates

Front 128

What are the nursing interventions for hypercalcemia?

Back 128

increase ambulation, encourage fluids (esp. with sodium if tolerated), fiber, watch for dig toxicity, cardiac rate and rhythm monitoring

Front 129

What is the most abundant intracellular cation after potassium?

Back 129

magnesium

Front 130

What does magnesium do?

Back 130

an activator for many intracellular enzymes (muscle contractility/excitability), involved in carbohydrate and protein metabolism, peripheral vasodilation

Front 131

What are normal serum magnesium levels?

Back 131

1.3-2.3 mEq/L

Front 132

Where is the serum magnesium?

Back 132

1/3 is bound to protein
2/3 is a free cation

Front 133

What can skew serum magnesium concentration measurements?

Back 133

albumin levels--must take these into consideration too

Front 134

What are causes of hypomagnesemia?

Back 134

alcohol withdrawal, diarrhea, fistula, ng suctioning, parental/tube feedings, diuretics, digitalis, cyclosporins, aminoglycosides, rapid admin of citrated blood, sepsis, burns, hypothermia, diabetic ketoacidosis

Front 135

How does small bowel disease, inflamm bowel disease, or intestinal restructuring affect hypomagnesemia?

Back 135

small bowel is major site of absorption, if not there, hypomagnesemia

Front 136

When do symptoms of hypomagnesemia occur?

Back 136

when serum mag level drops to < 1.0 mEq/L

Front 137

What are the s/s of hypomagnesemia?

Back 137

hyperexcitability, muscle weakness, tremors, twitching, tetany, pos Chvostek's and Trousseau's, prolonged QRS, depressed ST, cardiac dysrthymias, PVC, vent fib, apathy, depression, agitation, delirium, psychoses

Front 138

Why are is hypomagnesemia associated with digitalis toxicity?

Back 138

dig patients are likely to be taking diuretic too, predisposing them to renal loss of mag

Front 139

What is considered hypomagnesemia? And what is it associated with?

Back 139

1.3 mEq/L or 1.8 mg.dl
associated with hypokalemia and hypocalcemia

Front 140

What happens to the EKG with magnesium, calcium, potassium deficiencies?

Back 140

tachydysrhythmias, prolonged PR and QT interval, widening QRS, ST segment depression, flattened T wave, prominent U wave, PVC, torsades de pointes, paroxysmal atrial tachycardia, heart block

Front 141

How is hypomagnesemia treated?

Back 141

diet, magnesium salts, magnesium supp to parenteral nutrition, magnesium sulfate IV-- slow infusion

Front 142

What are nursing considerations for hypomagnesemia?

Back 142

low admin of magnesium IV/bolus, I/O, resp distress, hypotension, heart dysrythmias, seizure, dysphagia, deep tendon reflex, dig monitoring

Front 143

What causes hypermagnesemia?

Back 143

renal failure, excessive mag intake, adrenocortical insufficiency, Addison's diease, hypothermia, overuse of antacids, laxatives, decreased GI mobility, opiods, anticholinergis, lithium intoxication, diabetic ketoacidosis

Front 144

What are the clinical manifestations of hypermagnesemia?

Back 144

nausea, weakness, low BP, facial flushing, lethargy, difficulty speaking, resp depression, coma, AV block, platelet clumping, delayed thrombin formation

Front 145

What is considered hypermagnesemia?

Back 145

>2.5 mEq/L or 3.0 mg/dl

Front 146

What also occurs with hypermagnesemia?

Back 146

increased potassium and calcium, creatinine clearance <3.0 ml/min

Front 147

What are the EKG changes with hypermagnesemia?

Back 147

prolonged PR interval, tall T waves, widened QRS, prolonged QT, av block

Front 148

How is hypermagnesemia treated?

Back 148

removal of all magnesium salts, IV calcium gluconate, hemodialysis with mag free dialysate, loop diuretics, sodium cloride, lacted ringers,

Front 149

What are the nursing implications for hypermagnesemia?

Back 149

VS, I/O, hypotension, resp depression, decrease patellar reflexes, change in LOC, magnesium not given to renal failure patients

Front 150

What does phosphorus do?

Back 150

essential for muscle, RBC, ATP, 2,3-diphosphoglycerate (facilitates release of oxygen from hemoglobin), acid base balance, nervous system, metabolism of protein, fat, cho, structural support to bones and teeth

Front 151

What is a normal level of serum phosphorus?

Back 151

2.5-4.5 mg/dL (up to 6 for children who are growing)

Front 152

What is the difference between phosphorus deficiency and hypophosphatemia?

Back 152

phosphorus deficiency- abn low count of phosphorus in lean tissue with or without hypophosphatemia
Hypophosphatemia- below low normal serum phosphate

Front 153

What causes hypophosphatemia?

Back 153

IC shift of potassium into cells, malnutrition, alcoholism, pain, heat stroke, prolonged hyperventilation, diabetic ketoacidosis, hepatic encephalopathy, burns, chronic diarrhea, Vit D deficiency

Front 154

How does magnesium, potassium and parathyroid effect hypophosphatemia?

Back 154

low mag, low potassium, and hyperparathyroidism increase urinary loss of phosphorus

Front 155

What else can cause loss of phosphorus thru the kidneys?

Back 155

acute volume expansion, osmotic diuresis, carbonic anhydrase inhibitors, malignacies

Front 156

How does resp alkalosis effect phosphorus?

Back 156

resp alkalosis causes IC shift of phosphorus, decreasing phosphorus, from intracelluar glycolysis

Front 157

What are the clinical manifestations of hypophosphatemia?

Back 157

oxygen delivery deficiency--irritability, fatigue, weakness, numbness, paresthesia, seizure, coma, hypoxia, muscle damage, increase resp rate, impaired ventilation, bruising, acute rhabdomyolysis

Front 158

How is hypophosphatemia diagnosed?

Back 158

serum potassium < 2.5, may have osteomalacia, rickets

Front 159

What is the treatment for hypophosphatemia?

Back 159

phosphorus added to parental/enteral feeding, oral replacement, slow IV admin (10 mEq/L)

Front 160

What are nursing implications of hypophosphatemia?

Back 160

watch for potential dangers of IV admin of phosphorus--tetany, infiltration, infection, monitor serum levels, supplement, preventing infection (altered granulocytes)

Front 161

what is hyperphosphatemia?

Back 161

serum phosphate levels >4.5

Front 162

what causes hyperphosphatemia?

Back 162

renal failure, increase intake, decrease output, shift from intracellular to extracellular space, chemo, hypoparathyroidism, metab/resp acidosis, diabetic ketoacidosis, acute hemolysis, high phosphate intake, profound muscle necrosis, inc phosphate absorption

Front 163

What is the primary complication of hyperphosphatemia?

Back 163

metastatic calcification (soft tissues, joints, arteries)
-occurs when cal x mag = 70 mg/dl

Front 164

what are the s/s of hyperphosphatemia?

Back 164

tetany, anorexia, n/v, bone and joint pain, muscle weakness, tachycardia, hyperreflexia
-signs from low calcium and soft tissue calcification

Front 165

How is hyperphosphatemia treated?

Back 165

-find underlying disorder: vol depletion, resp/metab acidosis, renal failure, elevated PTH production
-vit D preparations (calcitriol), calcium binding antacids, phosphate binding gels/antacids, restriction of dietary phosphate, diuretics, dialysis, vol repletion with saline

Front 166

What are the nursing considerations for hyperphosphatemia?

Back 166

-low-phophorus diet (no hard cheese, nuts, meats, whole-grain cereal, dried fruit/veg)
-avoid laxatives that contain phosphate containing subst.
-signs of hypocalcemia

Front 167

What is the normal serum level of chloride and where is it found?

Back 167

-97-107 mEq/dl
-ECF, found esp in interstitial and lymph fluid in blood
-also found in gastric and pancreatic juices, sweat, bile, saliva

Front 168

What is chloride in direct relationship with and inversely related to?

Back 168

direct relationship to sodium
inversely related to bicarbonate

Front 169

Describe chlorides relationship to aldosterone and CSF?

Back 169

-aldosterone secretion increases sodium reabsorption as well as chlorides
-choroid plexus, where CFS is forms, depends on sodium and chloride to attract water to form the fluid portion

Front 170

How is chloride related to bicarbonate?

Back 170

as chloride moves from plasma to RBC, bicarbonate moves back into the plasma (H+ are then formed= acid base balance)

Front 171

How is chloride primarily obtained? Where is chloride produced?

Back 171

Thru the diet as table salt
-produced in the stomach, where it combines with H+ to form hydrochloric acid

Front 172

How is chloride controlled in the body?

Back 172

-intake
-excretion and reabsorption in the kidneys

Front 173

What can cause hypochloremia?

Back 173

GI tube drainage, severe vomiting/diarrhea, admin of chloride deficient formulas, low sodium intake, decrease sodium levels, metab alkalosis, prolonged IV therapy with dextrose, diuretics, burns, fever, admin of aldosterone, ACTH, corticosteroids, bicarbonate, or laxatives

Front 174

What happens as chloride decreases?

Back 174

sodium and bicarbonate ions are retained by the kidney to balance loss, bicarbonate accumulates in the ECF which raises the pH and leads to metab alkalosis

Front 175

What are the signs and symptoms of hypochloremia?

Back 175

-hyponatremia, hypokalemia, metabolic alkalosis (high pH and serum bicarb)
-PaCO2 >50 mmHg
-twitching, weakness, muscle cramps, hyperactive tendon reflexes, cardiac dysrthymias, seizures, coma

Front 176

How is hypochloremia diagnosed?

Back 176

electrolyte levels, ABG's, urine chloride level

Front 177

How is hypochloremia treated?

Back 177

NS or 0.45% NS, may discontinue diuretic, eat foods high in chloride, avoid free water, may give ammonium chloride

Front 178

What are the nursing interventions for hypochloremia?

Back 178

VS, I/O, LOC, serum electrolyte levels, muscular strength and movement, teach about foods high in chloride

Front 179

What is hyperchloremia?

Back 179

serum chloride >107
serum sodium >145
serum pH <7.35
serum bicarbonate <22
normal anion gap of 8-12

Front 180

What causes hyperchloremia?

Back 180

-loss of bicarb via kidneys or GI tract (chloride ions accumulate, acidosis results)
-head trauma, increase perspiration (cystic fibrosis, diabetes insipidus, glucose-6-phosphate deficiency, hypothyroidism, malnutrition, acute renal failure), excess adrenocortical hormone production, decreased GFR

Front 181

How is hyperchloremia treated?

Back 181

-correcting underlying cause, restoring F/E and acid balance
-hypotonic, LR, IV sodium bicarbonate
-diuretics
-sodium, chloride and fluid restriction

Front 182

What are the nursing interventions for hyperchloremia?

Back 182

VS, I/O, ABG's, teaching about diet, neuro/cardiac/resp assessment

Front 183

what is the pH range compatible with life?

Back 183

6.8-7.8

Front 184

What is the extracellular pH buffer system?

Back 184

bicarbonate-carbonic acid ration system

Front 185

How does CO2 effect carbonic acid?

Back 185

increase in CO2 causes increase in carbonic acid and vice versa

Front 186

How do the kidneys effect acidosis and alkalosis?

Back 186

acidosis-conserve bicarbonate and excrete H+
alkalosis-conserve H+ and excrete bicarbonate
-renal compensation is relatively slow

Front 187

How do the lungs effect acidosis and alkalosis?

Back 187

with an increase in CO2 (acidosis) respiration is stimulated to increase, with alkalosis respiratory rate decreases causing CO2 to be retained

Front 188

Define metabolic acidosis

Back 188

low pH (<7.35) and low bicarbonate (<22)
-cardial feature is decreased serum bicarbonate level

Front 189

What causes metabolic acidosis?

Back 189

bicarbonate loss: diarrhea, lower intestinal fistulas, ureterostomies, diuretics, early renal insufficiency, excessive administration of chloride, admin of parenteral nutrition without bicarbonate
Ketoacidosis, lactic acidosis, salicylate poisoning, uremia, methanol or ethylene glycol toxicity

Front 190

What are the s/s of metabolic acidosis?

Back 190

headache, confusion, drowsiness, increased resp rate and depth, n/v, peripheral vasodilation, decreased cardiac output (if pH is < 7.0), decreased BP, cold, clammy skin, dysrthymias, shock

Front 191

What causes chronic metabolic acidosis?

Back 191

chronic renal failure

Front 192

what may accompany metabolic acidosis?

Back 192

hyperkalemia (K shifts out of cell) followed by hypokalemia as acidosis is corrected
-hyperventilation decreases CO2 levels as a compensatory action

Front 193

How is metabolic acidosis treated?

Back 193

-bicarbonate is administered if pH < 7.1 or bicarb is <10
-Potassium is closely monitored
-in chronic conditions low serum calcium is treated before anything else
-hemodialysis or peritonial dialysis

Front 194

Define metabolic alkalosis?

Back 194

high pH (>7.45) and high plasma bicarbonate concentration (>26)

Front 195

What causes metabolic alkalosis?

Back 195

vomiting, gastric suctioning, pyloric stenosis, loss of potassium (diuretics), excessive adrenocorticoid hormones, excessive ingestion of antacids

Front 196

How does hypokalemia produce alkalosis?

Back 196

1. kidneys conserve K therefore H+ excretion increases
2. cellular K moves out of the cells into the ECF in an attempt to maintain near normal serum levels- H+ moves in to neutralize cell)

Front 197

What can cause chronic metabolic alkalosis?

Back 197

long term diuretic therapy, villous adenoma, external drainage of gastric fluids, K+ depletion, cystic fibrosis, chronic ingestion of milk and calcium carbonate

Front 198

What are the s/s of metabolic alkalosis?

Back 198

tingling of fingers and toes, dizziness, hypertonic muscles, hypocalcemia, respirations depressed (hypoventilation-hypoxemia), atrial tachycardia, ventricular disturbances, decreased motility and paralytic ileus, hypokalemia

Front 199

How can the difference between vomiting and diuretic therapy be distinguished from excessive adrenocorticosteroid secretion?

Back 199

-vomiting, cystic fibrosis, nutritional repletion, diuretic therapy, hypovolemia and hypochloremia produce urine chloride <25
-mineralocorticoid excess or alkali loading causes expaned fluid volume and urine chloride of >40

Front 200

How is metabolic alkalosis treated?

Back 200

suffient chloride is supplied so kidneys can absorb sodium and chloride (sodium chloride fluids), KCl to replace K+ and Cl- lost, tagamet given to reduce gastric HCl produced with gastric suctioning, carbonic anhydrase inhibitors for those who cannot tolerate rapid vol expansion

Front 201

Define respiratory acidosis?

Back 201

pH < 7.35 and PaCO2 >42
-inadequate excretion of CO2, hypoventilation

Front 202

What can cause respiratory acidosis?

Back 202

acute pulmonary edema, aspiration of a foreign object, atelectasis, pneumothorax, OD of sedatives, sleep apnea, admin of O2 to those with hypercapnia, pneumonia, acute respiratory distress syndrome, muscular dystrophy, myasthenia gravis, guillian-barre syndrome

Front 203

What are the s/s of respiratory acidosis?

Back 203

increased HR, respiratory rate, BP, mental cloudiness, fullness in the head, vasodilation causes increase of cerebral blood flow increasing intracranial pressure, papilledema, dilated conjuctival blood vessels, cyanosis, tachypnea ventricular fib, hyperkalemia

Front 204

What can cause chronic respiratory acidosis?

Back 204

obesity, sleep apnea, chronic emphysema, bronchitis
-those with COPD may not develop hypercapnia because compensatory renal changes have had enough time to occur

Front 205

What happens when a patient's PaCO2 is chronically >50?

Back 205

respiratory stimulant is hypoxemia (not CO2), thus giving them O2 may remove this stimulus and cause carbon dioxide narcosis.

Front 206

How is respiratory acidosis treated?

Back 206

directed at improving ventilation by removing what is impeding it.
-antibiodics, pharmacologics, thrombolytics, anticogulants, clear resp tract, adequate hydration, supplemental O2, mechanical ventilation, semi-fowler's position