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)
