Fluids & Electrolytes ppt (chap 24, 25) Flashcards
(83 cards)
1
Q
Define intracellular fluid
A
fluid within the cells
2
Q
Define extracellular fluid
A
all other body fluids
3
Q
Define interstitial fluid
A
fluid that lies between cells and tissues
4
Q
Define intravascular fluid
A
plasma within blood vessels
5
Q
Define transcellular fluid
A
cerebral spinal fluid, synovial fluid, peritoneal fluid
6
Q
Define osmosis. What are some characteristics of osmosis?
A
the movement of water across a semiperiable membrane. Fluid moves from LOW concentration to HIGH. Maintains fluid EQUILIBRIUM between fluid compartments
7
Q
Define osmolality
A
the concentration of solute (Na, K, Glucose, Urea) in a solvent (body water), reflects hydration status.
8
Q
What is the normal rage of serum osmolality?
A
280 – 300 mOsm/kg H20
9
Q
What is the normal rage of urine osmolality?
A
50-1200 mOsm/kg H20, random
10
Q
Define low serum osmolality. What causes a low serum osmolality?
A
higher than usual amount of water in relation to amount of particles dissolved. causes include overhydration, edema, SIADH, renal failure, diuretic use, adrenal insufficiency, high fluid intake.
11
Q
Define high serum osmolality? What causes a high serum osmolality?
A
less than usual amount of water in relation to amount of particles dissolved. causes dehydration, water loss, diabetes insipidus, hyperglycemia, hyperosmotic, hyperglycemic syndome, hypernatremia.
12
Q
What causes a low urine osmolality?
A
fluid volume excess, diabetes insipidus, acute renal failure, diuretic therapy
13
Q
What causes a high urine osmolality?
A
fluid volume deficit, SIADH, increaqsed ibuprofen use, dehydration, acidosis, shock
14
Q
What causes a low urine osmolality?
A
Fluid volume excess, diabetes insipidus, acute renal failure, diuretic therapy
15
Q
What are the starting forces?
A
capillary hydrostatic/oncotic pressure, interstitial hydrostatic/oncotic pressure
16
Q
Which starting forces shift fluid into the capillary? When can you see this?
A
capillary oncotic and interstitial hydrostatic. can be seen with HHANKS.
17
Q
Which starting forces shift fluid out of the capillary? When can you see this?
A
capillary hydrostatic and interstitial oncotic. can be seen in HF and cirrhosis
18
Q
How is fluid hemostasis regulated?
A
by thirst and renal excretion
19
Q
Explain how thirst regulates fluid hemostasis.
A
thirst is the primary regulator of water intake. the hypothalamus is stimulated by decreased fluid volume, increased serum osmolality, and high sodium balance
20
Q
Explain how the nervous system regulates fluid balance.
A
baroreceptors (detect pressure changes) pick up changes is arterial blood pressure and make changes as necessary. vasodilation and increased UO with high BP and vasoconstriction and decreased UO with low BP.
21
Q
Explain how aldosterone regulates fluid balance.
A
Low Na leads to an increase in ACTH which causes an increase in aldosterone. Aldosterone causes the body to hold onto Na and H2O increasing the fluid volume and BP (potent vasoconstrictor).
22
Q
Explain how ADH regulates fluid balance.
A
THE NO PEE HORMONE (tells body to hold unto H2O).
23
Q
Explain how RAAS regulates fluid balance.
A
RAAS leads to the release of angiotensin II which causes vasoconstriction which increases BP & perfusion. Aldosterone holds unto NA & H2O.
24
Q
What questions do you ask about the history of a pt w/ fluid electrolyte balance?
A
Does the pt have injury, disease, medications, dietary restrictions, total intake vs total output that alters f/e balance?
25
Explain how the nervous system regulates fluid hemostasis.
baroreceptors (detect pressure changes) pick up changes is arterial blood pressure and make changes as necessary. vasodilation and increased UO with high BP and vasoconstriction and decreased UO with low BP
26
Explain how aldosterone regulates fluid hemostasis.
aldosterone holds unto Na and H2O thus increasing the fluid volume and BP. aldosterone is stimulated by low Na
27
Explain how ADH regulates fluid hemostasis.
THE NO PEE HORMONE. Holds unto water. Stimulated by low lvls of fluid and increased osmolality
28
Explain how RAAS regulates fluid hemostasis.
Aldosterone is released which holds unto Na & H2O. Angiotennsin II is released which is a potent vasoconstrictor. All of this increased BP and fluid volume thus improving perfusion
29
What questions should the nurse ask about the pts history when assessing f/e balance?
Does pt have injury or disease that alters f/e balance? Medications that alter f/e balance? Dietary restrictions that alter f/e balance? Total intake versus total output?
30
What VS should the nurse be look for when assessing f/e balance?
Temp which could indicate fever from excess fluid loss and increased metabolic rate. Pulse to look for tachycardia that results from decreased intravascular volume or decreased Mg and K. Respirations that could indicate low K and Mg lvls which could cause respiratory muscle weakness. BP which could result in orthostatic hypotension from dehydration
31
What should the nurse be look for when performing the physical exam if f/e balance is suspected?
When inspecting look at the color, JVD, and mucous membranes. Palpate for skin turgor and cap refill. Look for signs of edema. Note the location and whether edema is pitting or non-pitting (+1 to +4). Auscultate for S3 or S4 heart sounds, pericardial friction rub, breath sounds. Percuss for ascities. Do a neuromuscular exam to assess for chvostek’s and trousseau’s sign, altered mental status, or tetany. Monitor hemodynamics for CVP, PAWP, CO, CI, MAP
32
What labs should the nurse be checking if f/e balance is suspected?
Serum Cr, BUN to Cr ratio, osmolality, anion gap which is the difference between CATIONS and ANIONS.
Determine cause of metabolic ACIDOSIS which could be increased with RENAL FAILURE.
Serum albumin, urine by doing either UA, urine volume, concentration, Cr clearance
33
How does the nurse manage f/e imbalances?
By performing routine labs per MD order/hospital protocol. Monitor lab values
Assess for s/sx of hypo/hyper states. Assess for s/sx of FVD/FVE. Cardiac monitoring. Daily wts. Awareness of medications, IVF, treatments, procedures that can cause imbalances
34
What are the manifestations of fluid volume excess?
Is fluid generalized or localized, edema (which could be the result of underlying condition), third-spacing (peritoneal - ascites, pleural, pericardia),
urine output can be DECREASED with FVExcess. Check the VS for increased BP, high CVP, increased CO. Altered mental status, JVD, edema, crackles that do not clear with cough, SOB, S3 or S4 heart sound, prei-orbital edema. Weight gain of 2.2 lbs (equals 1L H2O). Increased preload: PAP, wedge. Dec hct, low serum osmolality, xray – pulmonary congestion, pleural effusion, pericardial effusion, low urine specific gravity.
35
What is the treatment of fluid volume excess?
Treat cause and manifestations. Restrict fluid intake. Diuretics. Loop diuretics such as Furosemide (Lasix), Bumetadine (Bumex).
Thiazide diuretics such as
Hydrochlorothiazide (HCZ). Potassium sparing diuretics such as Spironolactone (Aldactone).
36
What are the causes of fluid volume deficit?
GI: N/V, nasogastric suction, fistulas, Ileostomy or colostomy
Urinary: Diuretics, uncontrolled diabetes, diabetes insipidus
Integumentary: Burns, diaphoresis, incr capillary permeability
Insensible: Inc RR, fever, inc metabolic rate, mechanical ventilation
Wound drainage
37
What are the manifestations of fluid volume deficit?
Hypotension, rapid WEAK, thready pulse, rapid, SHALLOW respirations, decr body temp. Dry mucous membranes, decr urine output, incr urine specific gravity, altered mental status, anxiety, decr LOC, dry skin, pale, decr skin turgor, sunken eye orbits
tachycardia, orthostatic hypotension, decr BP, decr cap refill
38
What is the treatment of fluid volume deficit?
Identify and control fluid loss.
REPLINISH fluids. Isotonic fluids such as D5W, 0.9% NS, or LR which can be used to tx intravascular deficits such as shock, trauma, fluid resuscitation. Hypotonic fluids such as 0.45% NS, 0.2% NS, or 2.5% dextrose which can be used to tx intercellular dehydration such as DKA, HHANKS.
Hypertonic fluids such as D51/2NS, D10W, or 3% NS which increases Na+ in bloodstream, brings interstitial fluid back into the vascular compartment. Used as volume expanders in hyponatremia. D20W used as an osmotic diuretic for cerebral edema
39
What are normal extracellular electrolytes?
Na, Cl, Ca
40
What are normal intracellular electrolytes?
K, Mg, PO4
41
What the normal ranges for Na, Cl, Ca, K, Mg, PO4
135-145, 90-105, 2.3-2.8, 3.5-5, 1.5-2.5, 1.7-2.7
42
Name some characteristics of sodium. How is it regulated? What is the normal intravascular and interstitial sodium?
Most abundant cation in ECF, helps with the transmission of impulses across muscle and nerve cells, maintain acid/base balance by combining with Cl or Bicarb to increase or decrease pH. Regulated by ADH and aldosterone. Normal intravascular Na is 142 & normal interstitial Na is 145.
43
Name some characteristics of hyponatremia.
44
Name some characteristics of hypernatremia.
>145, which leads to cell shrink. High amounts of Na can be caused by either high intake (diet, high NaHCO3 administration) or loss of water (diuretics, GI, fever)
45
What are the manifestations of hyponatremia?
HYPOtension, CONFUSION, HA, lethargy, SEIZURES, DECREASED muscle tone, muscle twitching, TREMORS, vomiting, diarrhea, cramping
46
What are the manifestations of hypernatremia?
HYPERtension, tachycardia, confusion, restlessness, SEIZURES, coma, hyperreflexia, muscle twitching, thirst (moderate incr Na+), coma, N/V
47
What is the treatment of hyponatremia?
Treat the underlying cause. If it was SIADH tx with IV NS. If severe hyponatremia give hypertonic saline (3, 5% NaCl), do not exceed 8-12 reduction of Na in 24 hr b/c at risk for neuro demyelination. PO fluid restriction
48
What is the nursing management of hyponatremia?
Risk for imbalanced fluid volume. Monitor for pulmonary and cerebral edema. Neuro changes from demyelination (dysphagia, seizures, death, spastic paresis). Monitor response to therapy
49
What is the treatment of hypernatremia?
Water replacement, hypotonic IV Fluids, diuretics, risk for injury
50
What is the nursing management of hypernatremia?
Neuro deterioration, monitor I&O, rapid neuro changes can cause CEREBRAL EDEMA
51
Name some characteristics of phosphorus. How is it regulated? What is the normal intracelluar phosphorus?
INTRAcellular mineral that is essential for teeth and bone development, normal NEUROMUSCULAR function, required for ATP production, protein, fat, and carb metabolism, pH balance, INVERSE relationship to Ca. Kidneys regulate levels by reabsorption & excretion of phosphorus. Normal intracellular phosphorus is 140
52
What are the manifestations of hypophosphatemia?
Weakness, numbness, tingling, pathologic fractures, diminished myocardial function,
N/V, anorexia, disorientation, irritability, seizures, coma, respiratory depression, respiratory muscle weakness. If severe there will be cardiac, respiratory, & nervous system dysfunction
53
What are the manifestations of hyperphosphatemia?
Muscle cramping, weakness, tachycardia
| D/N, abdominal cramping, similar to HYPOcalcemia
54
What is the treatment of hypophosphatemia?
Treat cause, replace levels, PO or IV supplements
55
What is the nursing management of hypophosphatemia?
Risk for injury, monitor for respiratory function, breathing patterns
56
What is the treatment of hyperphosphatemia?
Lower levels, binding agents, IV NS promotes renal excretion
57
What is the nursing management of hyperphosphatemia?
Monitor lab values and pt response to treatment
58
Name some characteristics of calcium. How is it regulated?
Stored in the BONE primarily. Required for: blood coagulation, neuromuscular contraction, enzymatic activities, bone integrity. Absorbed in GI tract under influence of VITAMIN D. Ca bound to PROTEINS in serum. Low ALBUMIN = low CALCIUM level and vice versa. 50% of Ca++ is ionized (not attached to proteins).
Ioinized Ca++ (ICa) used for PHYSIOLOGIC activities. Adults: 4.4 - 5.3 mg/dL which is critical for NEUROMUSCULAR activity.
ICa INVERSELY proportional to albumin so it's an important level to monitor. Regulated by PARATHYROID HORMONE (Calcitonin - when Ca lvls are high, Calcitriol - when Ca lvls are low ).
59
What causes hypocalcemia and hypercalcemia?
Hypocalcemia: Trauma, AKI, chronic kidney disease, sepsis, hypoparathyroidism, low magnesium levels, administration of Citate (stored BLOOD), acute pancreatitis.
Hypercalcemia: Primary hyperparathyroidism (causes ~ 50% of cases), immobilization (not frequent),
Vitamin A or D intoxication, breast or lung CA, multiple myeloma (MALIGNANT HYPERCALCEMIA)
60
What are the manifestations of hypocalcemia?
Muscle cramps, tetany, tingling/numbness, + Chvostek’s or Trousseau’s sign, tetany, irritable, decr cognition, seizures, EKG changes: incr QT inter-val, long ST segment, decr BP, decr myocardial contractility, LOW BP, abnormal clotting, bone fx, LAB: hyperphosphatemia
61
What are the manifestations of hypercalcemia?
GI: Anorexia, constipation, nausea, peptic ulcer disease
Neuro: Lethargy, depression, fatigue
Cardiac dysrhythmias, heart block, bradycardias, decr ST segment, HTN, pathologic bone fractures, bone thinning, kidney stones,
LAB: Hypophosphatemia
62
What is the treatment of hypocalcemia?
Correct underlying cause.
If present correct acidosis, before giving Ca+ to prevent tetany, cardiac arrest. IV calcium administration (Ca Gluconate preferred [Give SLOW IV], CaCl is 3x stronger)
63
What is the nursing management of hypocalcemia?
Monitor for other decreased electrolytes (Mg, K), risk for injury, monitor rhythm strips, decr CO, bradycardia, neuro & muscular changes
64
What is the treatment of hypercalcemia?
Correct underlying cause such as parathyroidectomy, chemo/ radiation of tumors.
Promote Ca elimination by:
IV Fluids, diuretics, biphosphantes, calcitonin, potassium phosphate
65
What is the nursing management of hypercalcemia?
Monitor for cardiac dysrhythmias, increase mobilization, encourage PP intake, assess environment for fracture risk
66
Name some characteristics of potassium. What is the normal intracellular K?
Intracellular CATION.
Most common electrolyte problem. Body sucks at handeling abnorml K+ levels, this can be potentially lethal.
Close monitoring required
K maintains CARDIAC & NEUROMUSCULAR function:
influences ACTION POTENTIAL of cardiac cells, affects muscle CONTRACTION, influence nerve impulse CONDUCTION. Regulates ACID-BASE balance. Normal intracellular K is 160
67
What are the causes of hypokalemia?
GI loss (vomiting/diarrhea, NG suction), diuretics without K+ supplementation, hyperaldosteronism (holds onto Na+, excretes K+)
68
What are the causes of hyperkalemia?
Associated with RENAL failure, metabolic acidosis which causes K moves out of cell, severe BURNS, rhabdomyolysis which causes cell death which then release of intracellular K+ and myoglobin from cell into bloodstream (electrical Burns, crush injury, statin meds)
69
What are the manifestations of hypokalemia?
Neuro: Confusion, depression, lethargy
Cardiac: PVC, Ventricular TachyDysrhythmias, Cardiac arrest
GI: N/V/D, decr bowel sounds, ileus
Musc: Paralysis, resp weakness, fatigue, leg cramps, muscle weakness, paresthesias.If taking Digoxin watch out for toxicity which is caused by hypokalemia
70
What are the manifestations of hyperkalemia?
Neuro: weakness, muscle cramps
GI: N/V/D, abdominal cramping
Cardiac: EKG changes, tachycardia to bradycardia to cardiac arrest, prolonged PR interval, peaked T wave, ST depression
Severe: VFIB, asystole, metabolic acidosis
71
What is the treatment of hypokalemia?
PO K administration (k-dUR), IV K+ administration:
| give KCL IV piggyback SLOW (10 mEq in 100 mL). Dose: 10 mEq over one hr
72
What is the nursing management of hypokalemia?
Monitor for decreased CO, monitor EKG’s, IV K through peripheral veins is painful (central IV best)
73
What is the treatment of hyperkalemia?
Treat underlying cause (K+ sparing diuretics, ACE inhibitors). Correct acidosis.
Regular insulin and D50W to move K back into cells. Kayexelate + Sorbitol (results unpredictable). Dialysis (severe)
74
What is the nursing management of hypercalcemia?
Risk for decr CO, EKG changes (peaked T wave), monitor BUN and Cr levels, renal function, check U/O
75
Name some characteristics of magnesium. What is the normal intracellular magnesium?
INTRAcellular electrolyte.
Helps with Na & K transport across cell membrane, needed for protein and carbohydrate metabolism, biochemical reactions & NERVE cell conduction, excreted in FECES and KIDNEYS. Closely related to K and Ca balance. Normal intracellular magnesium is 35
76
What are the causes of hypomagnesemia?
Acute pancreatitis, starvation, malabsorption syndrome, chronic alcoholism, burns
77
What are the causes of hypermagnesemia?
Rare. Diminished renal excretion, excessive antacids or laxatives
78
What are the manifestations of hypomagnesemia?
Tremors, tetany, + Chvostek’s and Trousseau’s signs, PVCs, V-tach, fibrillation, T wave flattened, decr ST segment
79
What are the manifestations of hypermagnesemia?
Absent DTRs, lethargy, drowsiness, hypotension, bradycardia, cardiac arrest, prolonged PR interval, complete heart block, wide QRS complex, depressed respiratory function
80
What is the treatment of hypomagnesemia?
Raise serum levels. IVF with Mg, Mg replacement – IV or PO
81
What is the nursing management of hypomagnesemia?
Risk for injury, monitor for ventricular dysrhythmias
82
What is the treatment of hypermagnesemia?
Identify cause, give calcium to lower Mg levels
83
What is the nursing management of hypermagnesemia?
Monitor for decreased CO, monitor for bradycardia, hypotension, EKG changes
