Transcript Fluid and Electrolytes All Slides

Electrolytes
ELECTROLYTE
REGULATION:
Cations **
Electrolyte
Regulation: Anions
 SODIUM
CHLORIDE
 Salt intake,
Aldosterone, Kidneys
 POTASSIUM
 Kidneys
 CALCIUM
 Parathyroid hormone
 MAGNESIUM
 Kidney
Kidneys
BICARBONATE
Kidneys
PHOSPHATE
Parathyroid
Kidneys,
Vitamin D
Hormone,
Activated
ELECTROLYTES: Memorize!!
 SODIUM
 Hyponatremia < 135 mEq/L
 Hypernatremia > 145 mEq/L
 POTASSIUM
 Hypokalemia < 3.5 mEq/L
 Hyperkalemia > 5.0 mEq/L
 Calcium
 Hypocalcemia < 8.5 mg/dl
 Hypercalcemia > 10.0 mg/dl
HYPONATREMIA
(Na < 135mEq/L)
 Overview
 controls water distribution (principle regulator of
extracellular fluid volume)
 necessary for nerve impulse transmission
alterations think “mental/neurological”
 Etiology
 loss of sodium: GI losses, diuretics, adrenal
insufficiency, sweating, or
 gain of water: edematous conditions, excessive
hypotonic fluids, SIADH (syndrome inappropriate
anti-diuretic hormone – covered in ENDO unit)
HYPONATREMIA (cont.)
 Physical Assessment/Clinical Manifestations
 (may include manifestations of dehydration)
 **altered mental status (increased water
content in brain cells!!) headache,
depression, personality changes, confusion,
lethargy, tremors leading to convulsions &
coma
 nausea, abd. cramps due to hyperactive
bowels, diarrhea
 muscle weakness, diminished deep tendon
reflexes
 Laboratory = Na< 135 mEq/L
Hyponatremia (cont.)
 Drug Therapy: Isotonic IV Fluids
 0.9% NaCl, Ringer’s Lactate or
 3% NaCl only with extreme caution
 Diet Therapy
 Provide Sodium Containing Foods; Restrict Water
 NURSING CARE
 Assess I&O, Weights, Monitor Fluid/GI Losses
 Monitor for Mental Changes; Safety
Where’s the Salt????
Refer to Table 11-6
review sources
 Obvious sodium (you can see it)
 Sodium as a flavor enhancer
 Sodium as a preservative
HYPERNATREMIA
(Na > 145 mEq/L
 Overview
 Basic problem = Inability to respond
to thirst
 Who is AT RISK?
 Young, old, or cognitively impaired
 Etiology (UNABLE TO RESPOND
TO THIRST)
 Administration of hypertonic
parenteral solutions or tube
feedings
 Excessive intake of sodium either
orally or through parenteral or
enteral feedings
 Excessive Intake of Sodium (very
excessive!)
Hypernatremia
 Physical Assessment/Clinical Manifestations




Dehydrated brain cells! Neurological/mental changes
Altered cerebral function (agitated, irritable, restless, unable to
concentrate) progressing to convulsions & coma
Thirst, (may have swollen dry tongue & sticky mucous membranes),
weight gain
Skeletal muscle weakness
 Laboratory = Na > 145 mEq/L
 Drug Therapy
 Hypotonic IV Solutions (0.45% NaCl)
 Water Replacement
 NURSING CARE




Monitor Fluid Gains & Losses, restrict sodium, give water
Monitor Changes in Behavior
Institute Safety Precautions
***Provide tap water to tube fed clients***
HYPOKALEMIA
 Overview
 Influences skeletal and CARDIAC activity
 Normal renal function is essential for balance
 Interesting facts:
 Potassium is the primary ICF cation so movement may
cause trouble &
 The kidneys regulate potassium & have trouble holding
onto it with some diuretics
 Fluid loss from the body usually includes potassium
since the body conserves it poorly
Hypokalemia (remember need on a
daily basis) K < 3.5 mEq/L
 Etiology: Actual Deficit
 Excessive loss due to:
 Diuretic use (think Loop Diuretics) (also other meds)

Especially with digitalis (will discuss in cardiovascular class)
 GI losses from diarrhea, vomiting, wound drainage, N/G
suction
 Heat-induced excessive diaphoresis
 Inadequate potassium intake:
 Prolonged NPO status
 Anorexia/starvation
 Etiology: Relative deficit
 Alkalosis with potassium shift into cells
 Hyperinsulinism, total parenteral nutrition (TPN)
 IV therapy without potassium
HYPOKALEMIA:
K < 3.5 mEq/L
 Physical Assessment/ Clinical Manifestations
 CARDIAC DYSRHYTHMIAS (heart beat irregular in
a bad way)
 Watch Digitalis (digoxin), hypokalemia
potentiates toxicity
 Generalized muscle weakness progressing to
paralysis
 Leg cramps, nausea & vomiting, paresthesias
 Decreased bowel sounds (paralytic ileus?)
 Decreased reflexes (hypo-reflexia)
 Laboratory = K < 3.5 mEq/L
HYPOKALEMIA
 Diet Therapy
 Food sources daily
 What is used in place of table salt (NaCl)?
 Why do we recommend orange juice or bananas?
 Know food sources of potassium (Table 11-7, p.
153)
 Drug Therapy
 Oral supplementation (caution can overdose)
 Know nursing implications for drugs such as K
Dur
 IV (never IV push, always mix & give with care,
check kidney function)
HYPERKALEMIA (> 5.0 mEq/L)
 Etiology


Excessive Potassium Intake
 Over-ingestion of food/medication
 Rapid infusion of IV containing potassium/bolus by
mistake
Decreased Potassium Excretion
 RENAL FAILURE/RENAL DISEASE
 Potassium sparing diuretics
 Adrenal insufficiency (more on that later)
 Etiology

Relative Potassium Excess (movement of K+ from
intracellular to extracellular space – temporary)
 Metabolic acidosis (Exchanges with H+)
(Diabetic ketoacidosis – more later)
 Marked tissue injuries (K+ released from cells)
KCL
HYPERKALEMIA (> 5.0 mEq/L)


Physical Assessment/Clinical Manifestations
 CARDIAC DYSRHYTHMIAS (heart can stop)
 Heightened neuromuscular activity, diarrhea, intestinal colic,
anxiety, paresthesias, irritability, muscle tremors & twitching
 Later: muscle weakness progressing to paralysis
Laboratory = K > 5.0 mEq/L
 HYPERKALEMIA: Drug Therapy
 Eliminate potassium administration by d/c IV with
K+, withhold oral K+, and avoid in diet.
 Increase potassium excretion by diuretics such as
Lasix, or use Kayexalate with Sorbitol (GI excretion
of K+, especially for clients with renal failure)
 Promote the movement of potassium back into the
ICF by giving Insulin or Hypertonic Dextrose
 & Sodium Bicarbonate (emergency measure
HYPOCALCEMIA < 8.5 mg/dl)
 Overview
 Most of total body calcium (99%) is found in bones &
teeth BUT not measured in blood calcium
 The remaining 1% is ionized & is measured in blood
calcium
 So Osteoporosis is NOT Hypocalcemia
 Osteoporosis is “brittle bones” & occurs after
inadequate calcium intake <age 30 or “runs in
families”
 Symptoms related to skeletal & muscle contraction
 Etiology
 Decreased parathyroid hormone
 Malabsorption of calcium (Pancreatitis, GI diseases)
 Marked deficiencies of dietary calcium and/or Vit D
 Laboratory = Ca < 8.5 mg/dl
HYPOCALCEMIA:
Physical Assessment/ Clinical Manifestations =
TETANY, paresthesias
•Bronchial muscle spasm, laryngospasm leading to
respiratory arrest
Hypocalcemia: Calcium Food
Sources (which 2 do not belong?
yogurt
cheese
broccoli
tofu
Ice cream
Cream cheese
Sardines
Spinach
Canned salmon
Skim milk
HYPOCALCEMIA <8.5 mg/dl
 Diet Therapy
 Food sources of Calcium (Table 11-8, p.
153) **know for exam
 Supplementation
 Drug Therapy
 Oral calcium
 IV Calcium (with caution)
 Vitamin D
 Interventions
 Protect from injury
HYPERCALCEMIA
>10.0 mg


Etiology

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
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Overuse of calcium supplements/antacids/Vit D
MALIGNANCY (why??)
Altered GI metabolism
Hyperparathyroidism



Decreased peristalsis resulting on constipation
Profound MUSCLE WEAKNESS, FLACCIDITY
Cardiac dysrhythmias
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Administer IV 0.9% NaCl (hemodilution)
Diuretics (excrete calcium & sodium)
Calcitonin & other calcium binding drugs

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
Dialysis
Cardiac Monitoring
Protect from injury
Avoid constipation
Physical Assessment/Clinical Manifestations
 Drug Therapy
 Interventions