Fluids & Electrolytes Pt 2 Flashcards
Sodium
- Imbalances typically assoc w/parallel changes in osmolality
- Plays a major role in
> ECF volume & concentration
> Generation & transmission of nerve impulses
> Muscle contractility
> Acid-base balance
- Serum sodium reflects ratio of sodium to water
- Changes in lvl may reflect a primary water imbalance, primary sodium imbalance, or combo
- Na+ leaves body through urine, sweat, & feces; kidneys as primary regulator
?
Elevated serum Na+ occurring w/water loss or Na+ gain
Causes hyperosmolality leading to ?
Primary protection is thirst from hypothalamus
Hypernatremia
cellular dehydration
A deficiency in the synthesis of release of ___ from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ___ (nephrogenic diabetes insipidus) can result in profound diuresis, producing a water deficit & hypernatremia
ADH
Manifestations
* Thirst, lethargy, agitation, seizures, & coma
- Impaired LOC
- Sx’s of fluid volume (deficit or excess ?)
deficit
If there’s an accompanying ECF volume deficit, manifestations like postural hypotension, weakness, & dec skin turgor occur
Analyze Cues Prioritize Hypotheses
- Risk for injury (! think of problems w/perfusion)
- Risk for fluid volume deficit (d/t water loss)
- Risk for electrolyte imbalance (d/t excessive intake of Na+)
- Potential complication: seizures & coma leading to irreversible brain damage
Planning & Implementation: Generate Solutions & Take Action
- Treat underlying cause
- Primary water deficit - replace fluid orally or IV w/isotonic or hypotonic fluids (D5W, 0.45% NaCl saline)
- Excess sodium - dilute w/Na+-free IV fluids (D5W) & promote excretion w/diuretics
- Monitor carefully
?
Results from loss of sodium-containing fluids &/or from water excess
Manifestations
> Confusion, irritability, HA, seizures, coma
Hyponatremia
Hyponatremia from loss of Na+-rich body fluids
- Profuse diaphoresis
- Draining wounds
- Excessive diarrhea or vomiting
- Trauma w/significant blood loss
Hyponatremia from water excess
- d/t inappropriate use of Na+-free or hypotonic IV fluids (>surgery, major trauma, fluid admin in renal failure pts)
! See CNS manifestations (cellular swelling)
Nursing Management Nursing Diagnoses
- Acute confusion
- Risk for injury
- Risk for electrolyte imbalance
- Potential complications: severe neurologic changes/irreversible damage
Generate Solutions & Take Action
- Caused by water excess
> Fluid restriction is needed
- Severe sx’s (seizures)
> Give small amts of IV hypertonic saline sol’n (3% NaCl)
- Abnormal fluid loss
> Fluid replacement w/Na+-containing sol’n
- Drugs that block vasopressin (ADH)
> Conivaptan (Vaprisol)
> Tolvaptan (Samsca)
?
Is used to treat hyponatremia assoc w/HF, liver cirrhosis, & SIADH
Tolvaptan (Samsca)
?
Results in inc urine output w/o loss of electrolytes like Na+ & K+
! Shouldn’t be used in pts w/hyponatremia from excess water loss
Conivaptan (Vaprisol)
?
- Major ICF cation (98% being ICF)
- Necessary for
> Transmission & conduction of nerve & muscle impulses
> Cellular growth
> Maintenance of cardiac rhythms (neuromuscular & cardiac function)
> Acid-base balance
Potassium
K+ conc in muscle cells is approx 140 mEq/L; in ECF 3.5 - 5.0 mEq/L
Needed for glycogen to be deposited in muscle & liver cells
Sources
- Fruits & vegetables (bananas & oranges)
- Salt substitutes
- K+ rx’s (PO, IV) [K+ penicillin]
- Stored blood
- Regulated by kidneys
> Eliminate 90% of K+ intake; rest lost in stool & sweat - Inverse relationship between Na+ & K+ reabsorption in kidneys
?
High serum K+ caused by
> Impaired renal excretion
> Shift from ICF to ECF
> Massive intake
- Most common in ?
Hyperkalemia
renal failure
Factors
> Adrenal insufficiency w/a subseq aldosterone deficiency
> Acidosis, massive cell destruction (burn or crush inj, tumor lysis, severe infections) & exercise
> Digoxin-like rx’s & beta-adrenergic blocking drugs (propranolol)
> Potassium-sparing diuretics (amiloride), aldosterone receptor blockers (spironolactone)
> ACE-inhibitors (enalapril, vasopril)
Hyperkalemia - Manifestations
- Cramping leg pain
- Weak or paralyzed skeletal muscles
- Abdominal cramping or diarrhea (d/t hyperactivity of smooth muscles)
- Cardiac dysrhythmias
- Inc conc of K+ outside cell, altering ICF:ECF; = inc cellular excitability
ECG effects of hyperkalemia
- P wave flattened; widening of QRS complex
- QT shortening & T wave more narrowed & peaked
Analysis: Analyze Cues
- Risk for activity intolerance & injury (r/t lower extremity muscle weakness)
- Risk for electrolyte imbalance
- Potential complication: dysrhythmias
- Eliminate oral & parenteral K intake
- Increase elimination of K (diuretics, dialysis, Kayexalate [oral/rectal])
Generate Solutions & Take Action
- Force K from ECF to ICF by IV insulin or sodium bicarbonate (<if acidotic)
- Reverse membrane effects of elevated ECF K+ by administering calcium gluconate IV
?
Low serum K+ caused by
- Inc loss of K+ via the kidneys or GI tract
- Inc shift of K+ from ECF to ICF
- Dietary K+ deficiency (rare)
- ___ deficiency
- Metabolic (acidosis or alkalosis ?)
Hypokalemia
Magnesium
alkalosis
Hypokalemia - Manifestations
! Cardiac most serious
* Skeletal muscle weakness (legs)
* Weakness of respiratory muscles
- Dec GI motility (= paralytic ileus or intestinal blockage)
- Impaired regulation of arteriolar blood flow
- Hyperglycemia (impairs insulin secretion)
ECG effects of hypokalemia
- T wave flattened; U wave emerging
- Peak in P waves; QRS complex prolonged
Analyze Cues
- Risk for activity intolerance & injury r/t muscle weakness & hyporeflexia
- Risk for electrolyte imbalance
- Potential complication: dysrhythmias
Generate Solutions & Take Action
- KCl supplements orally or IV
- Always dilute IV KCl
! NEVER give KCl via IVP or as a bolus
- Should not exceed 10 mEq/hr
> To prevent hyperkalemia & cardiac arrest
Calcium
- Formation of teeth & bone
- Blood clotting
- Transmission of nerve impulses
- Myocardial contractions
- Muscle contractions
- Obtained from ingested foods (or made in skin in presence of sun)
- Need vitamin D to absorb
- Present in 3 forms: ionized calcium is biologically active
- Changes in pH & serum albumin affect lvls
Changes in serum pH will alter the level of ionized Ca+ w/o altering the total Ca+ lvl
A decreased plasma pH (___) decreases Ca+ binding to ___, leading to more ionized Ca+
acidosis
albumin
An increased plasma pH (___) increases Ca+ binding, leading to decreased ionized Ca+
alkalosis
Calcium balance controlled by: (negative feedback)
- Parathyroid hormone
- Calcitonin
?
PTH is produced by the ____. Its production & release are stimulated by low serum Ca+ lvls
PTH increases bone resorption (movement of Ca+ out of bones), increases GI absorption of Ca+, & inc renal tubule reabsorption of Ca+
parathyroid gland
?
Is produced by the thyroid gland & is stimulated by high serum Ca+ lvls
Opposes action of PTH & lowers lvl of serum Ca+ by dec GI absorption, inc Ca+ deposition into bone, & promoting renal excretion
Calcitonin
?
High levels of serum Ca+ caused by
> Hyperparathyroidism (2/3 cases)
> Malignancy (myeloma, kidney/lung/breast ca’s)
> Prolonged immobilization
> Rare - vit D overdose or inc’d antacid ingestion
Hypercalcemia
Hypercalcemia - Manifestations
- Lethargy, weakness, stupor, coma
- Depressed reflexes
- Decreased memory
- Confusion, personality changes, psychosis
- Anorexia, N/V
- Bone pain, fx’s, nephrolithiasis
- Polyuria -> dehydration
Analyze Cues (! perfusion & safety)
- Risk for activity intolerance, electrolyte imbalance (r/t generalized muscle weakness & neuromuscular & sensorium changes)
- Risk for injury
- Potential complication: dysrhythmias (d/t dec myocardial excitability)
Generate Solutions & Take Action
- Excretion of Ca+ w/loop diuretic [furosemide]
> Drink 3000-4000 mL/day to excrete Ca+ & dec kidney stones forming - Hydration w/isotonic saline infusion
- Low Ca+ diet
- Mobilization
- Synthetic calcitonin (give IM or subq)
- Bi-phosphonates (Aredia, Zometa -> d/t malignancy; inhibit osteoclast activity)
?
Low serum Ca+ lvls caused by
- Dec production of PTH
- Acute pancreatitis (lipolysis is a consequence)
- Pts who receive many blood transfusions
- Alkalosis
- Inc Ca+ loss (i.e., from laxative abuse or malabsorption syndromes)
Hypocalcemia
Hypocalcemia - Manifestations
- Positive Trousseau’s or Chvostek’s sign
- Laryngeal stridor
- Dysphagia
- Tingling around the mouth or in the extremities
- Cardiac dysrhythmias (prolonged QT interval into a ventricular tachycardia)
?
Is a carpal spasm induced by inflating a BP cuff above the systolic pressure for a few min
Trousseau’s sign
?
Is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear
Chvostek’s sign
Analysis
- Acute pain (r/t tetany, sustained muscle contractions)
- Ineffective breathing pattern (d/t laryngospasms)
- Risk for electrolyte imbalance
- Risk for injury (d/t the tetany & seizures)
- Potential complication: Fx or respiratory arrest
- Treat cause
- Oral or IV Ca+ supplements
> Not IM to avoid local reactions - Rebreathe into paper bag (to promote CO2 retention)
- Treat pain & anxiety to prevent hyperventilation-induced respiratory alkalosis
?
- Coenzyme in metabolism of protein & carbs
- 2nd most abundant intracellular cation
- Req’d for nucleic acid & protein synthesis
- Helps maintain Ca+ & K+ balance
- Necessary for Na-K pump
Magnesium
- Acts directly on myoneural junction
- Important for normal cardiac function
- 50-60% contained in bone; 2% in ECF, rest in cell
- Absorbed in GI tract, excreted in kidneys
?
High serum Mg caused by
> Increased intake or ingestion of products containing Mg when renal insufficiency or failure is present
> Excess IV Mg admin
- In the pregnant woman who receives mag sulfate for preeclampsia
Hypermagnesemia
Hypermagnesemia - Manifestations
- Lethargy
- N/V
- Impaired reflexes
- Somnolence
- Resp & cardiac arrest
Management
- Prevent first - restrict Mg intake in high-risk pts
- Emergency treatment
> IV CaCl or calcium gluconate - Fluids & IV furosemide to promote urinary excretion
- Dialysis
?
Low serum Mg caused by
- Prolonged fasting or starvation
- Chronic alcoholism
- Fluid loss from GI tract
- Prolonged parenteral nutrition w/o supplementation
- Diuretics (inc risk of Mg loss through renal excretion)
- Hyperglycemic osmotic diuresis (uncontrolled DM inc renal excretion)
Hypomagnesemia
Hypomagnesemia - Manifestations
- Confusion / hyperactive DTRs
- Muscle cramps, tremors, seizures
- Cardiac dysrhythmias (PVC’s, v-fib)
- Corresponding ___ and ___
hypocalcemia; hypokalemia
Hypomagnesemia - Management
- Treat underlying causes
- Oral supplements
- Inc dietary intake (green vegetables, nuts, bananas, oranges, PB, chocolate)
- Parenteral IV or IM Mg when severe
